Shi, Yanan, Li, Bohan, Sun, Shuaifeng, Wendan, Tian, Ma, Zizhe, Liu, Wei. (1401). Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κB signaling pathway. , 26(1), 114-120. doi: 10.22038/ijbms.2022.67908.14848
Yanan Shi; Bohan Li; Shuaifeng Sun; Tian Wendan; Zizhe Ma; Wei Liu. "Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κB signaling pathway". , 26, 1, 1401, 114-120. doi: 10.22038/ijbms.2022.67908.14848
Shi, Yanan, Li, Bohan, Sun, Shuaifeng, Wendan, Tian, Ma, Zizhe, Liu, Wei. (1401). 'Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κB signaling pathway', , 26(1), pp. 114-120. doi: 10.22038/ijbms.2022.67908.14848
Shi, Yanan, Li, Bohan, Sun, Shuaifeng, Wendan, Tian, Ma, Zizhe, Liu, Wei. Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κB signaling pathway. , 1401; 26(1): 114-120. doi: 10.22038/ijbms.2022.67908.14848

Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κB signaling pathway

Iranian Journal of Basic Medical Sciences
مقاله 15، دوره 26، شماره 1، فروردین 2023، صفحه 114-120    اصل مقاله (1.09 M)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2022.67908.14848
نویسندگان
Yanan Shi1؛ Bohan Li2؛ Shuaifeng Sun1؛ Tian Wendan3؛ Zizhe Ma1؛ Wei Liu* 4
1Department of Cardiology, the Fourth Affiliated Hospital, Harbin Medical University, Harbin, PR. China, 150001
2Department of Cardiology, the Harbin Medical University, Harbin, PR. China, 150001
3Heilongjiang Provincial Hospital, Harbin, PR. China, 150001
4Department of Geriatric Cardiology, Guangdong Provincial People’s Hospital. Guangzhou, PR. China, 510080
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 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.
کلیدواژه‌ها
Cytokine؛ Inflammation؛ Myeloid differentiation- factor 88؛ Myocardial fibrosis؛ NF-κB؛ Toll-like receptor 4
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