Effects of astragalus polysaccharides on ventricular remodeling and miRNA-21 in rats with acute myocardial infarction

• 作者: Yang Dong Fen Zhang Xing-Xing Li Jie Wu Zhong-Cheng Xu
• 来源期刊: 海南医科大学学报（英文版）
• 年，卷（期）: 2021,（8）
• 所属期刊栏目: Original article
• 页码范围: 12-18
• 页数: 7页
• 语种: 英文

摘要

Objective: To investigate the effect of Astragalus polysaccharides (APS) on myocardial remodeling and expression of miR-21 after myocardial infarction. Methods: Sixty SPF grade healthy male rats were divided into the sham operation group, the model group, astragalus polysaccharide low, medium and high dose groups and atorvastatin group randomly with 10 rats in each group. The left anterior descending coronary artery (LAD) was ligated to establish myocardial infarction model in rats, and the corresponding drug intervention was given for 4 weeks. The changes of myocardial morphology and collagen were observed by HE and Masson staining. The levels of IL-1β, IL-6, TNF-α and IL-10 were detected by ELISA. The mRNA expressions of miR-21, MMP2, TIMP-2, Col-I, and Col-Ⅲ was detected by RT-PCR. The protein expressions of TLR4, MyD88 and NF-κB p65 were detected by Western blot. Results: Compared with the model group, APS could improve the pathological morphology of myocardial tissue, increase the level of IL-10 in myocardial tissue, reduce the staining area of collagen and the contents of IL-1 β, IL-6 and TNF-α (P<0.05). At the same time, APS could decreased the expression of MMP2, Col-I and Col-Ⅲ mRNA and the ratio of MMP2/TIMP-2, and increased the expression of TIMP-2 mRNA and miR-21 significantly (P<0.05). Furthermore, APS could significantly reduce the expression of TLR4, p-NF-κB p65 and MyD88 protein in myocardial tissue of rats with myocardial infarction, and the differences were statistically significant when compared with the model group (P<0.05). Conclusion: APS can inhibit the activation of TLR4/MyD88/NF-κB signaling pathway by upregulating the expression of miR-21, which plays a therapeutic role in ventricular remodeling after acute myocardial infarction.