科研之友
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摘要
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-I kappa B alpha, p-NF-kappa B, transforming growth factor beta 1 (TGF-beta 1), and alpha-smooth muscle actin (alpha-SMA) expression were detected by western blot. Inflammatory cytokines (IL-1 beta, IL-6, and TNF-alpha) in the serum were examined by ELISA. In the in vitro study, Ang II (1 mu mol/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-beta 1, and alpha-SMA expression in the myocardium. In the in vitro study, MGIIIE ameliorates the deposition of Col SIC and Col I and decreases the release of inflammatory cytokines. MGIIIE increased p-I kappa B alpha and reduced p-NF-kappa B expression both in vivo and in vitro. Conclusion: MGIIIE plays a role in anti-myocardial fibrosis, by inhibiting TLR4/MyD88/NF-kappa B signaling expression, and decreasing inflammatory cytokine release. MGIIIE may represent a novel therapeutic strategy for treating cardiac fibrosis.
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单位广东省人民医院; 哈尔滨医科大学
