این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
Iranian Journal of Basic Medical Sciences، جلد ۲۸، شماره ۶، صفحات ۷۱۰-۷۱۷

عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله

عنوان انگلیسی PGC-1α agonist ZLN005 ameliorates OVA-induced asthma in BALB/c mice through modulating the NF-κB–p65/NLRP3 pathway
چکیده انگلیسی مقاله Objective(s): Asthma is a complex inflammatory disease of the lungs marked by increased infiltration of leukocytes into the airways, which restricts respiratory function. Proliferator-activated receptor-γ coactivator-1 alpha (PGC-1α) has been recognized as an essential immunomodulator and has the potential as a novel anti-inflammatory target in asthma. The current study aims to investigate the functions of PGC-1α in ovalbumin (OVA)-sensitized asthmatic mice and underlying mechanisms.Materials and Methods: BALB/c mouse asthma model was induced by OVA in vivo. The therapeutic effects of PGC-1α agonist (ZLN005) on asthma were assessed by histological and biochemical analysis. In addition, we integrated real-time qPCR, western blotting, and immunofluorescence analysis to reveal the underlying mechanism.Results: In the lung tissue of asthmatic mice, PGC-1α levels were down-regulated. Diff-Quik staining indicated that ZLN005 therapy on asthmatic mice reduced the number of inflammatory cells (eosinophilic granulocytes, neutrophils, lymphocytes, and mononuclear macrophages) in bronchoalveolar lavage fluid (BALF), ameliorated pathologic alterations in lung tissues. ZLN005 alleviated airway structure and inflammation, as well as down-regulating the serum immunoglobulin E (IgE), OVA-specific IgE, and T-helper 2 (Th2) cytokines (interleukin (IL)-4, IL-5, and IL-13) expression. Mechanistically, the results showed that ZLN005, through the NF-κB-p65 axis, prominently inhibited the activation of the NLRP3 inflammasome and reduced the levels of the NLRP3 downstream targets IL-1β and IL-18.Conclusion: PGC-1α agonist (ZLN005) regulated lung inflammation in asthmatic mice by inhibiting the NF-κB-p65/NLRP3 signaling pathway, supporting that ZLN005 may be a candidate for future asthma treatment.
کلیدواژه‌های انگلیسی مقاله Asthma, Inflammation, NF-kappa B, NLR Family, Pyrin domain containing 3 - protein, Th2 cells

نویسندگان مقاله | Rui Fang
Department of Pediatrics, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, Anhui, China


| Yan Cheng
Department of Pediatrics, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, Anhui, China


| Ping Chen
Department of Pediatrics, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, Anhui, China


| Jing Hu
Department of Pediatrics, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, Anhui, China


| Liqi Yang
Department of Pediatrics, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, Anhui, China



نشانی اینترنتی https://ijbms.mums.ac.ir/article_25549.html
فایل مقاله فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده Original Article
برگشت به: صفحه اول پایگاه   |   نسخه مرتبط   |   نشریه مرتبط   |   فهرست نشریات