Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR۴/MyD۸۸/NF-κB signaling pathway
- سال انتشار: 1402
- محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 26، شماره: 1
- کد COI اختصاصی: JR_IJBMS-26-1_015
- زبان مقاله: انگلیسی
- تعداد مشاهده: 232
نویسندگان
Department of Cardiology, the Fourth Affiliated Hospital, Harbin Medical University, Harbin, PR. China, ۱۵۰۰۰۱
Department of Cardiology, the Harbin Medical University, Harbin, PR. China, ۱۵۰۰۰۱
Department of Cardiology, the Fourth Affiliated Hospital, Harbin Medical University, Harbin, PR. China, ۱۵۰۰۰۱
Heilongjiang Provincial Hospital, Harbin, PR. China, ۱۵۰۰۰۱
Department of Cardiology, the Fourth Affiliated Hospital, Harbin Medical University, Harbin, PR. China, ۱۵۰۰۰۱
Department of Geriatric Cardiology, Guangdong Provincial People’s Hospital. Guangzhou, PR. China, ۵۱۰۰۸۰
چکیده
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 C۵۷BL/۶ male mice (۶-۸ weeks) were randomly divided into a control group (n=۱۰), model group (n=۱۰), low MGIIIE dose group (n=۱۰), and high MGIIIE dose group (n=۱۰). Myocardial fibrosis was established by subcutaneous ISO injection. After ۲ 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 ۴ (TLR۴), myeloid differentiation factor ۸۸ (MyD۸۸), p-IκBα, p-NF-κB, transforming growth factor β۱ (TGF-β۱), and α-smooth muscle actin (α-SMA) expression were detected by western blot. Inflammatory cytokines (IL-۱β, IL-۶, and TNF-α) in the serum were examined by ELISA. In the in vitro study, Ang II (۱ μmol/l) was used to stimulate the fibroblasts, then inflammation and fibrosis index were detected.Results: MGIIIE inhibited inflammation and fibrosis and down-regulated TLR۴, MyD۸۸, TGF-β۱, 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 TLR۴/MyD۸۸/NF-κB signaling expression, and decreasing inflammatory cytokine release. MGIIIE may represent a novel therapeutic strategy for treating cardiac fibrosis.کلیدواژه ها
Cytokine, Inflammation, Myeloid differentiation- factor ۸۸, myocardial fibrosis, NF-κB, Toll-like receptor ۴اطلاعات بیشتر در مورد COI
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