این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
Iranian Journal of Basic Medical Sciences، جلد ۲۶، شماره ۱، صفحات ۱۱۴-۱۲۰
عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله
عنوان انگلیسی Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κB signaling pathway
چکیده انگلیسی مقاله Objective(s): To investigate the effect of mogroside IIIE (MGIIIE) on isoproterenol (ISO)-induced myocardial fibrosis and explore its possible mechanisms.Materials and Methods: Forty C57BL/6 male mice (6-8 weeks) were randomly divided into a control group (n=10), model group (n=10), low MGIIIE dose group (n=10), and high MGIIIE dose group (n=10). Myocardial fibrosis was established by subcutaneous ISO injection. After 2 weeks of continuous gastric administration of MGIIIE, the cardiac structure was evaluated by echocardiography. Myocardial inflammation and fibrosis were evaluated by histology examination. Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), p-IκBα, p-NF-κB, transforming growth factor β1 (TGF-β1), and α-smooth muscle actin (α-SMA) expression were detected by western blot. Inflammatory cytokines (IL-1β, IL-6, and TNF-α) in the serum were examined by ELISA. In the in vitro study, Ang II (1 μmol/l) was used to stimulate the fibroblasts, then inflammation and fibrosis index were detected.Results: MGIIIE inhibited inflammation and fibrosis and down-regulated TLR4, MyD88, TGF-β1, and α-SMA expression in the myocardium. In the in vitro study, MGIIIE ameliorates the deposition of Col Ш and Col I and decreases the release of inflammatory cytokines. MGIIIE increased p-IκBα and reduced p-NF-κB expression both in vivo and in vitro.Conclusion: MGIIIE plays a role in anti-myocardial fibrosis, by inhibiting TLR4/MyD88/NF-κB signaling expression, and decreasing inflammatory cytokine release. MGIIIE may represent a novel therapeutic strategy for treating cardiac fibrosis.
کلیدواژه‌های انگلیسی مقاله Cytokine, Inflammation, Myeloid differentiation- factor 88, myocardial fibrosis, NF-κB, Toll-like receptor 4
نویسندگان مقاله | Yanan Shi
Department of Cardiology, the Fourth Affiliated Hospital, Harbin Medical University, Harbin, PR. China, 150001


| Bohan Li
Department of Cardiology, the Harbin Medical University, Harbin, PR. China, 150001


| Shuaifeng Sun
Department of Cardiology, the Fourth Affiliated Hospital, Harbin Medical University, Harbin, PR. China, 150001


| Tian Wendan
Heilongjiang Provincial Hospital, Harbin, PR. China, 150001


| Zizhe Ma
Department of Cardiology, the Fourth Affiliated Hospital, Harbin Medical University, Harbin, PR. China, 150001


| Wei Liu
Department of Geriatric Cardiology, Guangdong Provincial People’s Hospital. Guangzhou, PR. China, 510080
نشانی اینترنتی https://ijbms.mums.ac.ir/article_21386.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