Abstract

In the present study, we assessed the therapeutic potential of Biochanin-A (BCA) (10 mg/kg BW/day) pretreatment for 30 days on lipid metabolic abnormalities, proinflammatory cytokines and matrix metalloproteinase expression in isoproterenol (ISO)-induced myocardial infarction (MI) in rats. We measured the potential role of BCA on tissue and circulatory lipid profiles as well as on lipid metabolic enzymes: serum inflammatory cytokines (TNF-α, IL-1α, IL-1β, IL-6 and MCP1) and serum Matrix Metalloproteinases (particularly, MMP-2 and MMP-9) together with mRNA expressions of TNF-α, IL-6, MMP-2 and MMP-9 by RT-PCR analysis. Administration of ISO to rats significantly distorted their lipid metabolism and augmented inflammatory process, MMP expression and proteolytic activity. In addition, pretreatment with BCA of ISO-induced MI rats significantly reestablished the altered lipid metabolism and concealed the inflammation of cytokines. BCA suppressed the expressions of proinflammatory cytokines and MMPs in ISO-induced MI in rats when compared to normal untreated MI rats. Hence, these results established that BCA could improve the pathological processes of myocardial remodeling which was confirmed by histopathology of heart in MI rats and might be an effective beneficial ingredient for the management of heart failure disorders.

摘要

在本研究中，我们评估了 Biochanin-A (BCA) (10 mg/kg BW/天) 预处理 30 天对异丙肾上腺素 (ISO) 诱导的心肌梗死中脂质代谢异常、促炎细胞因子和基质金属蛋白酶表达的治疗潜力(MI) 在大鼠中。我们测量了 BCA 对组织和循环脂质谱以及脂质代谢酶的潜在作用：血清炎性细胞因子（TNF-α、IL-1α、IL-1β、IL-6 和 MCP1）和血清基质金属蛋白酶（特别是， MMP-2 和 MMP-9) 以及通过 RT-PCR 分析的 TNF-α、IL-6、MMP-2 和 MMP-9 的 mRNA 表达。向大鼠施用 ISO 显着扭曲了它们的脂质代谢并增强了炎症过程、MMP 表达和蛋白水解活性。此外，用 BCA 对 ISO 诱导的 MI 大鼠进行预处理显着重建了脂质代谢的改变并掩盖了细胞因子的炎症。与未治疗的正常 MI 大鼠相比，BCA 抑制了 ISO 诱导的大鼠 MI 中促炎细胞因子和 MMP 的表达。因此，这些结果表明，BCA 可以改善心肌重塑的病理过程，这已被 MI 大鼠心脏的组织病理学证实，并且可能是治疗心力衰竭疾病的有效有益成分。