Publisher: Codon Publications   (Total: 3 journals)   [Sort by number of followers]

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Allergologia et Immunopathologia     Full-text available via subscription   (Followers: 2, SJR: 0.504, CiteScore: 1)
J. of Kidney Cancer and VHL     Open Access  
J. of Renal and Hepatic Disorders     Open Access  
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Allergologia et Immunopathologia
Journal Prestige (SJR): 0.504
Citation Impact (citeScore): 1
Number of Followers: 2  
 
  Full-text available via subscription Subscription journal
ISSN (Print) 0301-0546
Published by Codon Publications Homepage  [3 journals]
  • PHLDA1 knockdown inhibits inflammation and oxidative stress by regulating
           JNK/ERK pathway, and plays a protective role in sepsis-induced acute
           kidney injury

         This is an Open Access Article Open Access Article

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      Authors: Minmin Gong, Wenmei Liang, Qinju Lu, Jing Zhang
      Pages: 1 - 9
      Abstract: Background: Acute kidney injury (AKI), a prevalent complication of sepsis, causes substantial burden on patients’ families as well as the society. More reliable markers are urgently required for the prevention and treatment of AKI. Pleckstrin homology-like domain, family A, member 1 (PHLDA1) was implicated in various diseases, but its involvement in sepsis-induced AKI remains to be explored. The JNK/ERK pathway has been revealed as being involved in progression of sepsis. One previous study demonstrated that PHLDA1 could activate the JNK/ERK pathway in hepatic ischemia/reperfusion injury. Nevertheless, involvement of PHLDA1 in sepsis-triggered AKI through the JNK/ERK pathway has not been probed. Methods: A cecal ligation and punctured (CLP) mice model of sepsis-induced AKI was established. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunofluorescence staining were applied to evaluate the expression of PHLDA1. Concentration of blood urea nitrogen (BUN) and serum creatinine (Scr), inflammation markers, including interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α, as well as oxidative stress-associated proteins (catalase, malondialdehyde, superoxide dismutase, and glutathione), in the kidney tissues of mice were evaluated by enzyme-linked-immunosorbent serologic assay. Western blot analysis was applied for measuring protein expression levels. Results: The BUN and SCr levels in mice were obviously elevated in the CLP group compared to the sham group. Moreover, the expression of PHLDA1 was also elevated in the CLP group in comparison to the sham group. Down-regulation of PHLDA1 alleviated renal injury, inflammation, and oxidative stress in AKI model. Mechanistic study showed that PHLDA1 knockdown suppressed the activation of c-JUN N-terminal kinase/p38 and extracellular signal-regulated kinase (JNK/ERK) pathway. Conclusion: Down-regulation of PHLDA1 suppressed inflammation and oxidative stress through the modulation of JNK/ERK pathway in sepsis-induced AKI. The results could offer a novel insight into the treatment of patients with sepsis-induced AKI.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.671
      Issue No: Vol. 50, No. 6 (2022)
       
  • Vitamin D deficiency in children and adolescents with food allergy:
           

         This is an Open Access Article Open Access Article

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      Authors: Andressa Perez dos Santos Pereira, Raquel Bicudo Mendonça, Fernando Luiz Affonso Fonseca, Márcia Carvalho Mallozi, Roseli Oselka Saccardo Sarni
      Pages: 10 - 16
      Abstract: Our objective was to describe the serum vitamin D concentrations of children and adolescents with food allergy (FA) and to verify the association between the number of food allergens involved, length of sun exposure, and nutritional status. Through a cross-sectional study, 79 patients with FA, from ages 2 to 15 years, were assessed and followed up in a reference outpatient clinic, in Sao Paulo, Brazil. Clinical and biochemical data were collected for analysis of 25(OH)D, calcium, phosphorus, phosphatase, parathyroid hormone (PTH), and high-sensitivity C-reactive protein (hs-CRP). The cut-off point used for vitamin D deficiency was 25(OH)D ≤ 20 ng/mL. Vitamin D deficiency was detected in 45.6% of patients with a median age of 6.9 years (Interquartile range [IQR] 4.7; 10.2). The median serum 25(OH)D concentration was 21.1 ng/mL (IQR 17.8; 26.0). Multivariate linear regression was performed considering serum vitamin D level as a dependent variable. Allergy to multiple foods (inverse) and length of sun exposure (direct), but not nutritional status, were independently associated with serum 25(OH)D levels (P = 0.034 and P = 0.014, respectively). Patients with cow’s milk allergy also showed lower vitamin D concentrations in comparison with other FA (19.1 ng/mL [IQR 16.6; 24.4] vs 22.2 ng/mL [IQR 18.1; 27.1] [P = 0.056]). Vitamin D deficiency affected about half of individuals with FA. Multiple food allergy was associated with lower vitamin D concentrations, reinforcing the importance of monitoring vitamin D status in patients with FA.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.571
      Issue No: Vol. 50, No. 6 (2022)
       
  • A new autoimmune disease: atopic dermatitis in children
         This is an Open Access Article Open Access Article

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      Authors: Emanuela Floca, Remus Gaga, Genel Sur, Iulia Lupan, Ionel Armat, Samasca Gabriel, Lucia Sur
      Pages: 17 - 21
      Abstract: Atopic dermatitis (AD) is mainly considered an allergy, exacerbated by allergic factors. Is there evidence to suggest the existence of autoimmune components in the pathophysiology of the illness' Studies in the literature that dealt with the occurrence of autoimmunity in children with AD were analyzed. We followed the studies published in PubMed for 10 years, from 2001 to 2021. Clinical signs and symptoms were similar to other autoimmune diseases, having periods of remission and relapses. Other correlations between AD and autoimmune diseases have been described, and patients with AD can also present with a wide range of autoimmune comorbidities. Three major factors contribute to the pathogenesis of AD: damage of the skin barrier, disorders of the immune response, and imbalances of the skin microbiome—all based on genetic changes and influenced by environmental factors. Predominant activation of Th 2 cells, with the increase of Th 1, Th 17, and Th 22 subsets, promotes skin inflammation. All this evidence suggests that AD might be classified as an autoimmune disease, not just as an allergic reaction.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.655
      Issue No: Vol. 50, No. 6 (2022)
       
  • High throughput virtual screening strategy to develop a potential
           treatment for bronchial asthma by targeting interleukin 13 cytokine
           signaling

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      Authors: Qin Ma, Huimin Tong, Junhu Jing
      Pages: 22 - 31
      Abstract: Chronic inflammation in the airway passage leads to the clinical syndrome of pediatric asthma. Allergic reactions caused by bacterial, viral, and fungal infection lead to the immune dis-balance which primes T helper cells (Th2), a specific cluster of differentiation 4 (CD4) T cell differentiation. This favors the Th2-specific response by activating the inter-leukin 4/interleukin 13 (IL-4/IL-13) cytokine signaling and further activates the secretion of immunoglobulin E (IgE). IL-13 develops bronchial asthma by elevating bronchial hyperresponsiveness and enables production of immunoglobulin M (IgM) and IgE. The present study aims to target IL-13 signaling using molecular docking and understanding molecular dynamic simulation (MDS) to propose a compelling candidate to treat asthma. We developed a library of available allergic drugs (n=20) and checked the binding affinity against IL-13 protein (3BPN.pdb) through molecular docking and confirmed the best pose binding energy of –3.84 and –3.71 for epinephrine and guaifenesin, respectively. Studying the interaction of hydrogen bonds and Van der Walls, it is estimated that electrostatic energy is sufficient to interact with the active site of the IL-13 and has shown to inhibit inflammatory signaling. These computational results confirm epinephrine and guaifenesin as potential ligands showing potential inhibitory activity for IL-13 signaling. This study also suggests the designing of a new ligand and screening of a large cohort of drugs, in the future, to predict the exact mechanism to control the critical feature of asthma.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.573
      Issue No: Vol. 50, No. 6 (2022)
       
  • Whole-exome sequencing identified a homozygous novel RAG1 mutation in a
           child with omenn syndrome

         This is an Open Access Article Open Access Article

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      Authors: Wendi Wang, Jian Wang, Jingjing Wang, Jingting Liu, Jianying Pei, Wanyi Li, Yanxia Wang, Santasree Banerjee, Ruifeng Xu, Bin Yi
      Pages: 32 - 46
      Abstract: Introduction and objectives: Omenn syndrome (OS) is a very rare type of severe combined immunodeficiencies manifested with erythroderma, eosinophilia, hepatosplenomegaly, lymphadenopathy, and elevated level of serum IgE. OS is inherited with an autosomal recessive mode of inheritance. Germline mutations in the human RAG1 gene cause OS.
      Materials and methods: In this study, we investigated a 2-month-old boy with cough, mild anaemia, pneumonia, immunodeficiency, repeated infection, feeding difficulties, hepatomegaly, growth retardation, and heart failure. Parents of the proband were phenotypically normal. Results: Karyotype analysis and chromosomal microarray analysis found no chromosomal struc-tural abnormalities (46, XY) and no pathogenic copy number variations (CNVs) in the proband. Whole-exome sequencing identified a novel homozygous single nucleotide deletion (c.2662delC) in exon 2 of the RAG1 gene in the proband. Sanger sequencing confirmed that both the proband parents were carrying this variant in a heterozygous state. This variant was not identified in two elder sisters and one elder brother of the proband and in the 100 ethnically matched normal healthy individuals. This novel homozygous deletion (c.2662delC) leads to the frameshift, which finally results in the formation of the truncated protein (p.Leu888Phefs*3) V(D)J recombination-activating protein 1 with 890 amino acids compared with the wildtype V(D)J recombination-activating protein 1 of 1043 amino acids. Hence, it is a loss-of-function variant. Conclusions: Our present study expands the mutational spectrum of the RAG1 gene associated with OS. We also strongly suggested the importance of whole-exome sequencing for the genetic screening of patients with OS.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.529
      Issue No: Vol. 50, No. 6 (2022)
       
  • Omalizumab and allergen immunotherapy for respiratory allergies
         This is an Open Access Article Open Access Article

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      Authors: Maria De Filippo, Martina Votto, Lucia Caminiti, Francesco Carella, Giovanna De Castro, Massimo Landi, Roberta Olcese, Ilenia Panasiti, Mario Vernich, Salvatore Barberi, Giorgio Ciprandi, Gian Luigi Marseglia
      Pages: 47 - 52
      Abstract: Although currently approved to treat severe asthma and chronic spontaneous urticaria, omalizumab has also been an effective and safe add-on treatment for other allergic diseases. Namely, omalizumab has been proposed to be used as add-on therapy in patients with allergic rhinitis and asthma and undergoing specific allergen immunotherapy (AIT). AIT is the only treatment that modifies the natural history of IgE-mediated diseases. This brief review summarizes the available evidence and controversies on the efficacy and safety of omalizumab combined with specific AIT.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.495
      Issue No: Vol. 50, No. 6 (2022)
       
  • CTRP6 suppresses neutrophil extracellular traps formation to ameliorate
           sepsis-induced lung injury through inactivation of ERK pathway

         This is an Open Access Article Open Access Article

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      Authors: Jing Li, Ruijing Xuan, Weidong Wu, Yang Han, Jiani Guo, Meixia Yang
      Pages: 53 - 59
      Abstract: Background: Septic lung injury is associated with excessive neutrophil activation, while neutrophil extracellular traps formation contributes to inflammatory lung injury in sepsis. C1q/tumor necrosis factor–related protein-6 (CTRP6) is a paralog of adiponectin and exerts anti-inflammatory and antioxidant properties. The role of CTRP6 in sepsis-associated inflammatory lung injury was investigated in this study. Methods: Mice were injected with lipopolysaccharides (LPS) intraperitoneally to establish the mouse sepsis model. They were first tail-vein injected with adenovirus-mediated overexpression CTRP6 (Ad-CTRP6) and then subjected to the LPS injection. Pathological changes in lungs were detected by hematoxylin and eosin staining. Inflammation cytokine levels in bronchoalveolar lavage fluid were assessed by qRT-PCR and ELISA. Flow cytometry was used to detect the number of neutrophils in bronchoalveolar lavage fluid, and immunofluorescence was performed to assess neutrophil extracellular traps. Results: Lipopolysaccharides induced pulmonary congestion, interstitial edema, and alveolar wall thickening in the lungs, as well as upregulated lung histology score and wet/dry weight ratio. CTRP6 was reduced in lung tissues of septic mice. Injection with Ad-CTRP6 ameliorated extensive histopathological changes in LPS-induced mice and decreased lung histology score and wet/dry weight ratio. Overexpression of CTRP6 reduced the levels of TNF-α, IL-6, and IL-1β in septic mice. Injection with Ad-CTRP6 also decreased the number of neutrophils and downregulated Cit-H3 and myeloperoxidase polymers in septic mice. Protein expression of p-ERK in septic mice was reduced by overexpression of CTRP6. Conclusion: CTRP6 attenuated septic lung injury, exerted anti-inflammatory effect, and suppressed neutrophil extracellular traps formation against sepsis through inactivation of extracellular signal-regulated kinase signaling.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.677
      Issue No: Vol. 50, No. 6 (2022)
       
  • Serum dual-specificity phosphatase 1 reflects decreased exacerbation risk,
           correlates with less advanced exacerbation severity and lower inflammatory
           cytokines in children with asthma

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      Authors: Xingqing Guo, Chong Wang, Dong Xie, Cui Bai, Chenggang Mao, Fang Wang
      Pages: 60 - 67
      Abstract: Background: It is as fact that dual-specificity phosphatase 1 (DUSP1) regulates the T cell activation, pro-allergic response, and inflammation to engage with the pathogenesis of asthma, but its clinical role in children with asthma is unclear. The present study aimed to explore the expression of DUSP1, its association with exacerbation risk, severity, and inflammatory cytokines in children with asthma. Method: Around 52 children with asthma-exacerbation, 50 children in asthma-remission, and 50 healthy children were chosen for the study. The serum levels of DUSP1, as well as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and IL-17 were detected by the enzyme-linked immunosorbent assay. Results: The levels of DUSP1 was the highest in healthy children (median (IQR)=34.305 (25.892– 43.693) ng/mL), the second highest in children in asthma-remission (median (IQR)=21.471 (18.581–27.934) ng/mL), and the lowest in children with asthma-exacerbation (median (IQR)=13.982 (7.901–21.624) ng/mL) (P<0.001). At the same time, DUSP1 was also related to decreased asthma risk with area under curve (AUC) (95%CI) of 0.847 (0.780–0.914), and correlated with its lower exacerbation risk with AUC (95%CI) of 0.755 (0.661–0.849). Besides, DUSP1 was negatively linked with exacerbation severity (rs=–0.338, P=0.014), immunoglobulin E (rs=-0.277, P=0.047), TNF-α (rs=-0.423, P=0.002), IL-1β (rs=-0.389, P=0.004), and IL-17 (rs=-0.293, P=0.035), but not related with other disease features in children with asthma-exacerbation. Meanwhile, DUSP1 was only negatively associated with TNF-α (rs=-0.300, P=0.034) and IL-1β (rs=-0.309, P=0.029) in children in asthma-remission. However, no correlation was found in DUSP1 with inflammatory cytokines or other disease features in healthy children (all P>0.05). Conclusion: DUSP1 reflects the reduced exacerbation risk, and associates with lower exacerbation severity and inflammatory cytokines in children with asthma-exacerbation; it also associates with inflammatory cytokines in children in asthma-remission. These findings suggest that DUSP1 may help to improve the management of asthmatic children.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.575
      Issue No: Vol. 50, No. 6 (2022)
       
  • Contact dermatitis from black henna tattoo in child due to
           paraphenylenediamine

         This is an Open Access Article Open Access Article

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      Authors: Francisca Cunha, Iolanda Alen Coutinho, Carmelita Ribeiro, Ana Todo Bom
      Pages: 68 - 70
      Abstract: Temporary henna tattoos have become increasingly popular, particularly among children and teenagers. The word “henna” is of Persian origin, and it is prepared from the plant Lawsonia inermis belonging to the family Lythraceae. Concerning allergic reactions, natural henna paste is rarely responsible for contact dermatitis, which is more frequent if paraphenylenediamine (PPD) is added to the paste. The authors present a case of female child with erythematous exanthems that appeared after the application of black henna tattoo. A diagnosis of contact dermatitis to black henna tattoo was hypothesised. Epicutaneous tests were performed at the Immunoalergology Department of the Coimbra University Hospital using standard European battery and natural henna paste. The tests revealed positive reaction to PPD.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.597
      Issue No: Vol. 50, No. 6 (2022)
       
  • Anti-inflammatory effect of N-(trifluoromethylphenyl)-
           2-cyano-3-hydroxy-crotonic acid amide and gluconic acid on allergic
           rhinitis and asthma controlling

         This is an Open Access Article Open Access Article

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      Authors: Xing Liu, Entezar Mehrabi Nasab, Seyyed Shamsadin Athari
      Pages: 71 - 75
      Abstract: Allergic rhinitis and asthma are the main airway diseases with a higher prevalence. Eosinophilic inflammation, airway hyperresponsiveness, mucus hypersecretion, and reversible airflow obstruction are immunopathogenesis symptoms of rhinitis and asthma. Crotonic acid has bio-activity on the inflammation, and gluconic acid as chelator may protect crotonic acid activity in airway and together may control allergic rhinitis and asthma. Allergic rhinitis and asthma mice models were treated with crotonic and gluconic acids. The total IgE, histamine, IL-4, IL-5, and IL-13 levels were measured. In lung tissues, goblet cell hyperplasia, mucus hypersecretion, and inflammation were evaluated. The level of IL-5, goblet cell hyperplasia, and perivascular and peribronchial inflammation were controlled by crotonic acid in asthma and allergic rhinitis groups. But, total IgE, hista-mine, IL-4, and IL-13 levels, and mucus hypersecretion had no significant changes between treated and nontreated asthma and rhinitis groups. Crotonic acid can control eosinophilic inflammation via harnessing IL-5 and preventing goblet cell hyperplasia. When used with gluconic acid, it had a strong effect on the control of allergic rhinitis and asthma immunopathologies.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.612
      Issue No: Vol. 50, No. 6 (2022)
       
  • Research progress of statins on immune regulation of multiple sclerosis
           and experimental allergic encephalomyelitis

         This is an Open Access Article Open Access Article

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      Authors: Dongsheng Xu, Manxia Wang
      Pages: 76 - 83
      Abstract: Objective: The aim of this study is to summarize studies on statins used to treat multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE) and its underlying mechanisms. Methods: We searched some representing databases. Some studies were included if the effects of statins were tested on MS and EAE. The methodological quality was evaluated by the Collaborative Approach to Meta-Analysis and Review of Animal Data from Experimental Studies checklist. Results: Studies have confirmed that statins have immunomodulatory, neuroprotective and anti-inflammatory effects, and can be used in combination with immunomodulators of different mechanisms to treat MS and EAE. Statins have been shown to improve the following symptoms MS, reduce the number of attacks and the number of lesions, through immunomod-ulatory, neuroprotective and anti-inflammatory effects, and has a good safety profile. Conclusions: In short, statins represent an attractive new measure for treating MS. Some studies indicate that in addition to immunomodulatory effects, statins may have neuroprotective and neuro-repairing effects. The combination of statins with other immunosuppressive drugs has also produced encouraging results. This can be broadly prospects prospected to treat MS and EAE. It is hoped that in the near future, a combination of statins with less adverse reactions and high efficacy combined with other immunomodulators will bring exact results to patients with MS.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.658
      Issue No: Vol. 50, No. 6 (2022)
       
  • Protopine alleviates lipopolysaccharide-triggered intestinal epithelial
           cell injury through retarding the NLRP3 and NF-κB signaling pathways to
           reduce inflammation and oxidative stress

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      Authors: Junyu Li, Zhongjun Xu, Canhui OuYang, Xiongjian Wu, Yun Xie, Jun Xie
      Pages: 84 - 92
      Abstract: Background: Inflammatory bowel disease (IBD) is a common chronic intestinal disease. Protopine isolated from different plants has been investigated to understand its special functions on varied diseases. However, the regulatory effects of protopine on the progression of IBD remain unclear. Our study is aimed to explore the effects of protopine on the progression of IBD and its underlying regulatory mechanism of action. Methods: The cell viability was assessed through MTT colorimetric assay. The protein expressions of genes were examined by Western blot analysis. The cell apoptosis and reactive oxygen species level were measured using flow cytometry. The levels of inflammation and oxidative stress-related proteins were tested through enzyme-linked-immunosorbent serologic assay. The intracellular Ca2+ concentration and mitochondrial membrane potential were measured through immunofluorescence assay. Results: First, different concentrations of lipopolysaccharide (LPS) were treated with NCM460 cells to establish IBD cell model, and 5-μg/mL LPS was chosen for followed experiments. In this study, we discovered that protopine relieved the LPS-induced inhibited intestinal epithelial cell viability and enhanced cell apoptosis. Moreover, protopine attenuated LPS-stimulated inflammation activation and oxidative stress. Further experiments illustrated that the increased intracellular Ca2+ concentration and decreased mitochondrial membrane potential stimulated by LPS were reversed by protopine treatment. Finally, through Western blot analysis, it was demonstrated that protopine retarded the activated NLR family pyrin domain containing 3 (NLRP3) and nuclear factor kappa B (NF-κB) signaling pathways mediated by LPS. Conclusion: Protopine alleviated LPS-triggered intestinal epithelial cell injury by inhibiting NLRP3 and NF-κB signaling pathways to reduce inflammation and oxidative stress. This discovery may provide a useful drug for treating IBD.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.669
      Issue No: Vol. 50, No. 6 (2022)
       
  • Morroniside alleviates lipopolysaccharide-induced inflammatory and
           oxidative stress in inflammatory bowel disease by inhibiting NLRP3 and
           NF-κB signaling pathways

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      Authors: Shifen Zhang, Qiaohua Lai, Liming Liu, Yajie Yang, Juan Wang
      Pages: 93 - 99
      Abstract: Objective: To investigate the effects of morroniside on inflammatory and oxidative stress in lipopolysaccharide (LPS)-induced inflammatory bowel disease (IBD) cell model. Methods: NCM460 cells were treated with 2-, 5-, or 10-μg/mL LPS for 24 h to develop an IBD cell model. MTT (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) colorimetric assay was performed to uncover the role of morroniside on the viability of LPS-treated NCM460 cells. Flow cytometry and immunoblot assays were performed to confirm the effects of morroniside on the apoptosis of LPS-treated NCM460 cells. Quantitative polymerase chain reaction and enzyme-linked-immunosorbent serologic assays were performed to confirm the effects of morroniside on inflammatory and oxidative stress by measuring the levels of tumor necrosis factor-α, interleukin-1β, IL-6, superoxide dismutase, malondialdehyde, total antioxidant capacity, and myeloperoxidase. In addition, immunoblot and immunofluorescence assays were performed to detect the effects of morroniside on NLRP3 and NF-κB pathways. Results: Monosine attenuated LPS-induced injury of NCM460 cells. Monosine reduced LPS-induced inflammation in NCM460 cells. In addition, morroniside reduced LPS-induced oxidative stress in NCM460 cells. Mechanically, morroniside suppressed NLRP3 and NF-κB pathways, and alleviated LPS-induced inflammatory and oxidative stress in IBD. Conclusion: Morroniside could serve as a promising drug for treating IBD.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.674
      Issue No: Vol. 50, No. 6 (2022)
       
  • Does the asthma-chronic obstructive pulmonary disease overlap syndrome
           (ACOS) exist' A narrative review from epidemiology and practice

         This is an Open Access Article Open Access Article

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      Authors: David L. Hahn
      Pages: 100 - 106
      Abstract: Asthma and chronic obstructive pulmonary disease (COPD) have traditionally been approached as separate entities that must be researched and treated separately. There is growing recognition, however, that a substantial proportion of patients with obstructive lung disease have characteristics of both asthma and COPD (termed the asthma–COPD overlap syndrome (ACOS)). Lung disease experts have difficulty defining ACOS, and many still resist accepting the possibility that asthma and COPD may be linked. It is likely that practicing clinicians may be equally confused about how to identify and treat ACOS. This narrative review aims to clarify concepts of ACOS definition, argues that the best way to understand ACOS is to view the chronic lung disease process longitudinally rather than cross-sectionally, and presents evidence that ACOS can be the end result of the natural history of severe asthma. The review also points out the serious gaps in knowledge regarding therapy for ACOS and presents emerging data supporting the intracellular respiratory pathogen Chlamydia pneumoniae as a possible common etiologic agent in severe asthma and ACOS.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.678
      Issue No: Vol. 50, No. 6 (2022)
       
  • Anethole ameliorates inflammation induced by monosodium urate in an acute
           gouty arthritis model via inhibiting TLRs/MyD88 pathway

         This is an Open Access Article Open Access Article

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      Authors: Yuepeng Cao, Qin Zhong, Fang Tang, Xueming Yao, Zhengqi Liu, Xiaodong Zhang
      Pages: 107 - 114
      Abstract: Objective: To assess the effects of anethole on monosodium urate (MSU)-induced inflammatory response, investigate its role in acute gouty arthritis (AGA), and verify its molecular mechanism. Methods: Hematoxylin and eosin staining assay and time-dependent detection of degree of ankle swelling were performed to assess the effects of anethole on joint injury in MSU-induced AGA mice. Enzyme-linked-immunosorbent serologic assay was performed to demonstrate the production levels of inflammatory factors (interleukin 1β [IL-1β], interleukin 6 [IL-6], interleukin 8 [IL-8], tumor necrosis factor α [TNF-α], and monocyte chemo-attractant protein-1 [MCP-1]) in MSU-induced AGA mice. Western blot assays were used to confirm the effects of anethole on oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activity and the activation of toll-like receptors (TLRs)–myeloid differentiation factor 88 (MyD88) pathway in MSU-induced AGA mice. Results: We observed that a significant joint injury occurred in MSU-induced AGA mice. Anethole could alleviate the pathological injury of the synovium in MSU-induced AGA mice and suppressed ankle swelling. In addition, we observed that anethole could inhibit MSU-induced inflammatory response and inflammasome activation in MSU-induced AGA mice. Moreover, we discovered that anethole enabled to inhibit the activation of TLRs/MyD88 pathway in MSU-induced AGA mice. Our findings further confirmed that anethole contributed to the inhibitory effects on progression in MSU-induced AGA mice. Conclusion: It confirmed that anethole ameliorated the MSU-induced inflammatory response in AGA mice in vivo via inhibiting TLRs–MyD88 pathway.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.682
      Issue No: Vol. 50, No. 6 (2022)
       
  • Knockdown of Bcl-3 alleviates psoriasis and dyslipidemia comorbidity by
           regulating Akt pathway

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      Authors: Wei Li, Wei Yang, Can Yang
      Pages: 115 - 121
      Abstract: Background: Psoriasis is considered as an inflammatory skin disease accompanied by dyslipidemia comorbidity. B-cell leukemia-3 (Bcl-3) belongs to IκB (inhibitor of nuclear factor kappa B [NF-κB]) family, and regulates inflammatory response through associating with NF-κB. The role of Bcl-3 in psoriasis was investigated in this study. Methods: Apolipoprotein E (ApoE)-deficient mice were treated with imiquimod to induce psoriasis and dyslipidemia. Mice were injected intradermally in the back with lentiviral particles encoding Bcl-3 small hairpin RNA (shRNA). Hematoxylin and eosin were used to detect pathological characteristics. The blood lipid levels were determined by automatic biochemical analyzer, and inflammation was assessed by enzyme-linked-immunosorbent serologic assay and real-time quantitative reverse transcription polymerase chain reaction. Results: Bcl-3 was elevated in imiquimod-induced ApoE-deficient mice. Injection with lentiviral particles encoding Bcl-3 shRNA reduced Psoriasis area and severity index (PASI) score in ApoE-deficient psoriatic mice. Knockdown of Bcl-3 also ameliorated imiquimod-induced psoriasiform skin lesions in ApoE-deficient mice. Moreover, loss of Bcl-3 enhanced expression of loricrin, an epidermal barrier protein, reduced expression of proliferating cell nuclear antigen (PCNA) and lectin-like oxidized LDL (oxLDL) receptor-1 (LOX-1) in imiquimod-induced ApoE-deficient mice. The enhanced levels of blood lipid in ApoE-deficient mice were attenuated by silencing of Bcl-3 with increase of high-density lipoprotein, and reduction of total cholesterol, triglycerides, and low-density lipoprotein cholesterol. Knockdown of Bcl-3 attenuated imiquimod-induced decrease of transforming growth factor beta (TGF-β), and increase of Interleukin (IL)-17A, IL-23, IL-6, and tumor necrosis factor-α (TNF-α) in ApoE-deficient mice. Protein expression of phospho-Akt (p-Akt) and p-GSK3β in ApoE-deficient psoriatic mice was decreased by silencing of Bcl-3. Conclusion: Loss of Bcl-3 exerted anti-inflammatory effect on psoriasis and dyslipidemia comorbidity through inactivation of Akt/GSK3β pathway.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.683
      Issue No: Vol. 50, No. 6 (2022)
       
  • A new classification option for NSAID hypersensitivity
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      Authors: Ebru Özdemir, Ebru Damadoğlu, Gül Karakaya, A. Fuat Kalyoncu
      Pages: 122 - 127
      Abstract: Background: The European Network for Drug Allergy (ENDA) proposed a consensus document for hypersensitivity reactions to nonsteroidal anti-inflammatory drugs (NSAIDs) in 2011. A subgroup of patients with NSAIDs-exacerbated respiratory disease (NERD) develop urticaria/ angioedema type reactions in response to NSAIDs. The Kalyoncu classification might be a novel option to classify patients with NSAID hypersensitivity (NH). In this study, we compare the ENDA and the Kalyoncu classifications.
      Methods: This study enrolled a total of 196 patients. NH reaction types were categorized as asthma, rhinitis, urticaria/angioedema and anaphylaxis. Based on the reaction history and oral provocation test findings, patients were grouped according to ENDA and Kalyoncu classifications. Results: The mean age of the 196 patients was 40.32±13.28 years, and 130 (66.3%) of them were female. Under the ENDA and Kalyoncu classifications, the most common NH subgroups were NERD (32%), and isolated NH (34.2%), the least prevalent NH subgroups were single NSAID-induced delayed reactions (SNIDR) (1.5%), and pseudo Samter’s syndrome (11.7%). Conclusions: Our research revealed that the Kalyoncu classification is more descriptive of patients with NERD exhibiting urticaria/angioedema-type reactions. It also provides future risk assessment for development of NERD. For controversial cases, the Kalyoncu classification can be utilized as a new complimentary option alone or in conjunction with ENDA classification.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.693
      Issue No: Vol. 50, No. 6 (2022)
       
  • Study of the specificity of gut microbiota in adult patients with
           delayed-onset of atopic dermatitis

         This is an Open Access Article Open Access Article

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      Authors: Ting Liu, Chuan Yang, Jia He, Yujuan Wang, Tengyao Hu, Xiaoxiao Zhang
      Pages: 128 - 136
      Abstract: Background: Atopic dermatitis (AD) is a common and recurrent skin disease. The first onset of AD in adults is known as adult-onset atopic dermatitis (AOAD). Gut microbiota is closely associated with AD, and the “gut–skin” axis is considered as a novel target for prevention of AD. However, only a few studies have analyzed AOAD, particularly the studies that compared differences in intestinal flora between AOAD and persistent AD patients.
      Objective: To investigate main specificities of intestinal microbiota in AOAD patients, particularly comparing with persistent AD patients. Methods: A comprehensive taxonomic and functional analysis of gut microbiota in 10 healthy, 12 AOAD, and 10 persistent AD patients was done by using bacterial 16S ribosomal RNA (rRNA) gene analysis. Chao1 and Shannon diversity indices were measured to analyze alpha diversity, and the linear discriminant analysis (LDA) effect size (LEfSe) algorithm was applied to identify differences in genus. Results: The alpha diversity of gut microbiota in AOAD patients was decreased, with Escherichiashigella (15.8%) being the predominant genus of AOAD group. Agathobacter and Dorea in AOAD patients were significantly reduced, whereas the relative level of Bacteroides pectinophilus group was remarkably elevated compared with healthy volunteers and persistent AD patients. Conclusion: The present study revealed differences in intestinal flora between AOAD, healthy adults, and non-adult onset of AD, and explored differential dominant bacteria between AOAD and persistent AD patients.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.705
      Issue No: Vol. 50, No. 6 (2022)
       
  • Therapeutic potentials of the caffeine in polycystic ovary syndrome in a
           rat model

         This is an Open Access Article Open Access Article

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      Authors: Amir Raoofi, Mohammad Jafar Rezaie, Ali Delbari, Seyed Amir-Hossein Ghoreishi, Pegah Hadi Sichani, Shahram Maleki, Davood Nasiry, Maedeh Akhlaghi, Vahid Ebrahimi, Amin Mousavi Khaneghah
      Pages: 137 - 146
      Abstract: Recent studies have shown that polycystic ovary syndrome (PCOS) affects about 6% of women worldwide. It is associated with reproductive and metabolic dysfunction. Caffeine is naturally found in tea, cocoa, and coffee. It has been shown that caffeine can change hormonal profiles, stimulate ovulation, and enhance fertility. Therefore, in this study, the effects of caffeine on rats with PCOS were investigated. For this purpose, 40 female rats were divided into five groups: (1) control group (without any intervention), (2) sham group (administration of olive oil as a caffeine solvent), (3) PCOS group (injection of 2 mg of estradiol valerate for each rat), (4) caffeine group (administration of 37.5 mg/kg caffeine for each rat), and (5) PCOS + caffeine group. After 21 days of treatment, the ovaries of rats were removed and prepared for further evaluations, including hematoxylin and eosin staining, TUNEL assay, real-time PCR, and biochemical analysis. Administration of caffeine in PCOS mice considerably reduced both the volume of the ovary (P < 0.05) and follicular clusters (P < 0.01). However, superoxide dismutase and glutathione peroxidase were dramatically active in the PCOS + caffeine group compared to others (P < 0.05). Besides, caffeine treatment in PCOS mice led to Bax reduction and increased Bcl-2 expression. On the other hand, the expression of IL-6 and TNF-α in PCOS + caffeine group was high compared to other groups. We found that caffeine can reduce apoptosis and inflammation in PCOS ovaries and enhance the unpleasant symptoms of PCOS.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.715
      Issue No: Vol. 50, No. 6 (2022)
       
  • Urolithin A induces protective autophagy to alleviate inflammation,
           

         This is an Open Access Article Open Access Article

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      Authors: Xingli Cao, Hong Wan, Hao Wan
      Pages: 147 - 153
      Abstract: Objective: To investigate the therapeutic effect of urolithin A (UA) on pediatric pneumonia and the underlying mechanisms. Methods: The pediatric infantile pneumonia model was constructed by intratracheal induction of lipopolysaccharide (LPS) in 1-week-old C57BL/6 mice (male, 4–5 g). UA was also injected intraperitoneally. Lung tissues in each group were examined by histological analysis. Autophagy, inflammation, and oxidative stress were assessed by enzyme-linked-immunosorbent serologic assay and immunoblot analysis. Moreover, pyrophosis and endoplasmic reticulum stress were also evaluated by immunoblot analysis. Results: UA alleviated lung inflammation in mice, and inhibited cell pyrophosis. In addition, UA A relieved both oxidative and endoplasmic reticulum stress. Furthermore, we found that UA alleviated pneumonia damage by inducing protective autophagy.
      Conclusion: UA induced protective autophagy to alleviate inflammation, oxidative stress, and endoplasmic reticulum stress in pediatric pneumonia.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.743
      Issue No: Vol. 50, No. 6 (2022)
       
  • Orientin inhibits the progression of fibroblast-like synovial cells in
           rheumatoid arthritis by regulating MAPK-signaling pathway

         This is an Open Access Article Open Access Article

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      Authors: Weiqin Ji, Wei Xu
      Pages: 154 - 162
      Abstract: Background: Natural compounds are found to play an essential role in diverse inflammatory diseases, including rheumatoid arthritis (RA). Orientin, a flavonoid compound, is closely related to diverse pathological processes. Nevertheless, the role of orientin in RA is still unknown. Methods: The cell viability was tested through cell counting kit 8 (CCK-8) assay, and the number of cell colonies was calculated via colony formation assay. In addition, flow cytom-etry assay was employed to detect apoptosis rate in human RA fibroblast-like synoviocytes (RA-FLS). Besides, Transwell assay was introduced to determine cell migratory and invasive abilities. Moreover, the level of cytokines (IL-8, IL-1β, and IL-6) was estimated with quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent serologic assay. Furthermore, western blotting analysis was used to test the protein levels of cleavedcaspase-3, Bax, BCL-2, matrix metalloproteinase (MMP)-2, MMP-9, phosphorylated c-Jun N-terminal kinase, p-P38, and phospho-extracellular signal-related kinase. Results: Orientin inhibited cell viability, migration as well as invasion in a concentration-dependent manner in human RA-FLS. Additionally, treatment of orientin facilitated apoptosis and decreased the secretion of cytokines induced by tumor necrosis factor alpha (TNF-α) in human RA-FLS. Moreover, orientin inactivated mitogen-activated protein kinase (MAPK)-related signaling pathway, notably in human RA-FLS.
      Conclusion: These findings confirmed that orientin inhibited human RA-FLS development and decreased TNF-α-induced inflammatory factors, at least partly, by modulating MAPK-signaling pathway, which implied that orientin might be an effective agent for treating RA.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.742
      Issue No: Vol. 50, No. 6 (2022)
       
  • Analysis of response of severe eosinophilic asthmatic patients to
           benralizumab

         This is an Open Access Article Open Access Article

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      Authors: Juan Carlos Miralles-López, Rubén Andújar-Espinosa , Francisco Javier Bravo-Gutiérrez, Manuel Castilla-Martínez, Isabel Flores-Martín, María Loreto Alemany-Francés, Manuel José Pajarón-Fernández, Ana Mora-González, Sheila Cabrejos-Perotti, Zouhair El-Molaka, José Meseguer-Arce, María Jesús Avilés-Inglés, José Valverde-Molina, Virginia Pérez-Fernández, RE-ASGRAMUR GROUP
      Pages: 163 - 168
      Abstract: Introduction: Clinical trials and real-life studies have been published showing effectiveness of benralizumab in severe eosinophilic asthmatic patients. The aim of the present study is to describe super-responders to benralizumab in a series of 79 patients who completed at least 1 year of treatment, and to compare super-responders with non super-responders. Methods: This is a multicenter study of the Register of Severe Asthma of the Region of Murcia (RE-ASGRAMUR) Group performed in eight hospitals under the conditions of routine clinical practice. Patients with zero exacerbations and no oral corticosteroid therapy for asthma were considered super-responders. We analyzed clinical, functional, and inflammatory parameters of selected patients.
      Results: In all, 50 of the 79 patients (63%) met the super-responder criteria. In addition, 36% of the patients (26/71) were considered as complete responders to treatment (superresponder + Asthma Control Test [ACT] ≥ 20 + forced expiratory volume in 1 s [FEV1] ≥ 80%). The super-responders were significantly older in age (P = 0.0029), had higher eosinophils count (P = 0.0423), higher proportion of nasal polyps (P = 0.036), and they had less severe disease at baseline. After 1 year of treatment, the super-responders had higher levels of ACT questionnaire (23 vs 19, P = 0.0007) and better percentage of FEV1 (83 vs 75, P = 0.0359). Conclusion: Almost two of the three patients treated with benralizumab were super-responders after 1 year of treatment and 36% had a complete response. Super-responders were associated with older age, higher eosinophils count, had nasal polyposis as comorbidity, and had less severe disease at baseline. This data illustrated the good real-life response of patients with severe eosinophilic asthma to the treatment with benralizumab.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.704
      Issue No: Vol. 50, No. 6 (2022)
       
  • Knockdown of DAPK1 attenuates IL-1β-induced extracellular matrix
           degradation and inflammatory response in osteoarthritis chondrocytes via
           regulating the p38 MAPK-signaling pathway

         This is an Open Access Article Open Access Article

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      Authors: Jie Wei, Chen Gao, Ke Hu, Mingyue Li, Jingshi Li, Mengman Shen, Shuyu Zhang
      Pages: 169 - 175
      Abstract: Objective: To reveal the possible effects of death-associated protein kinase 1 (DAPK1) on the progression of osteoarthritis (OA) and the potential underlying mechanism. Methods: The expression of DAPK1 in OA and normal samples and interleukin (IL)-1β-stimulated chondrocytes was analyzed by quantitative real-time polymerase chain reaction and Immunoblot assay. Cell viability, proliferation, and apoptosis in DAPK1-knockdown cells stimulated with IL-1β were detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) solution, 5-ethynyl-2′-deoxyuridine staining and flow cytometry. The chondrocyte degradation and inflammatory response in IL-1β-induced chondrocytes were investigated by Immunoblot analysis and enzyme-linked-immunosorbent serologic assay. In addition, the effect of DAPK1 on p38 mitogen-activated protein kinase (MAPK) activation was analyzed by immunoblot assay. Results: This study revealed that DAPK1 was highly expressed in OA patients and IL-1β-induced chondrocytes. Down-regulation of DAPK1 enhanced IL-1β-induced chondrocyte proliferation. DAPK1 knockdown inhibited IL-1β-induced chondrocyte degradation. In addition, DAPK1 depletion inhibited IL-1β-induced chondrocyte inflammation. Mechanically, it was revealed that down-regulation of DAPK1 could inhibit the p38 MAPK pathway, and therefore affected progression of OA. Conclusion: DAPK1 knockdown attenuates IL-1β-induced extracellular matrix degradation and inflammatory response in OA chondrocytes by regulating the p38 MAPK pathway.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.744
      Issue No: Vol. 50, No. 6 (2022)
       
  • Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis
           in alveolar type II epithelial and bronchial epithelial cells by
           activating pulmonary surfactant proteins A and D

         This is an Open Access Article Open Access Article

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      Authors: Yun Shi, Huaiqing Yin
      Pages: 176 - 186
      Abstract: Background: Injury to the lung is a common, clinically serious inflammatory disease. However, its pathogenesis remains unclear, and the existing treatments, including cytokine therapy, stem cell therapy, and hormone therapy, are not completely effective in treating this disease. Dimethyl itaconate (DMI) is a surfactant with important anti-inflammatory effects. Objective: The present study used alveolar type II (AT II) and bronchial epithelial cells as models to determine the role of DMI in lung injury. Material and Methods: First, the effects of DMI were established on the survival, inflammatory release, and apoptosis in lipopolysaccharide (LPS)-induced AT II and bronchial epithelial cells. The association between DMI and Sirtuin1 (SIRT1) was assessed using molecular docking. Next, by constructing interference plasmids to inhibit surfactant protein (SP)-A and SP-D expressions, the effect of DMI was observed on inflammatory release and apoptosis. Results: The results revealed that DMI increased the survival rate and expression levels of SP-A, SP-D, and SIRT1, and inhibited inflammatory factors as well as apoptosis in LPS-induced cells. Furthermore, DMI could bind to SIRT1 to regulate SP-A and SP-D expressions. After SP-A and SP-D expressions were inhibited, the inhibitory effect of DMI was reversed on inflamma-tory release and apoptosis. Conclusion: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.586
      Issue No: Vol. 50, No. 6 (2022)
       
  • IRX1 ameliorates sepsis-induced acute kidney injury in mice by promoting
           CXCL14

         This is an Open Access Article Open Access Article

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      Authors: Jie Zhang, Yanlin Yue, Yunyan Ma
      Pages: 187 - 194
      Abstract: Background: Sepsis-induced acute kidney injury is a general critical complication having high relevance to kidney inflammation. In spite of advances in clinical and critical care, the specific and effective therapies for acute kidney injury are still insufficient. The present study aimed to investigate the protective effect of Iroquois homeobox genes (IRX) on sepsis-induced kidney dysfunction in mice. Methods: In order to gain insight into sepsis-related actions in acute kidney injury, the cecal puncture-induced kidney injury animal model was established. The hematoxylin and eosin staining was used to measure the pathology of kidney tissues. The kidney function-related biomarkers, including neutrophil gelatinase-associated lipocalin, creatinine, kidney injury molecule-1, blood urea nitrogen, and inflammatory cytokines, which included tumor necrosis factor α, interleukin 1β (IL-1β), IL-6, and monocyte chemotactic protein 1, were detected by automated biochemical analyzer or their corresponding test kits. The protein expression was measured using Western blot analysis, and the apoptotic rate of kidney tissue was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Results: The present study revealed the protective ability of IRX1 in sepsis-induced acute kidney injury. This study also determined the potential mechanism of IRX1 on sepsis-induced inflammatory response and cell apoptosis. Finally, it highlighted that IRX1 exerted a protec-tive influence on CLP-induced acute kidney injury by suppressing the activation of chemokine (C-X-C motif) ligand 14 (CXCL14). Conclusion: To conclude, the results suggest that overexpression of IRX1 could promote survival rate and suppress the CLP-induced apoptosis, inflammatory response, and kidney dysfunction through the activation of CXCL14. IRX1 and CXCL14 are essential to elucidate the mechanism of acute kidney injury. These findings may help to identify the promising targets for clinical sepsis therapy.
      PubDate: 2022-11-01
      DOI: 10.15586/aei.v50i6.733
      Issue No: Vol. 50, No. 6 (2022)
       
 
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