Ursolic acid modulates MMPs, collagen-I, α-SMA, and TGF-β expression in isoproterenol-induced myocardial infarction in rats

被引：38

作者：

Radhiga, T. ^{[1
]}

Senthil, S. ^{[1
]}

Sundaresan, A. ^{[1
]}

Pugalendi, K. V. ^{[1
]}

机构：

[1] Annamalai Univ, Dept Biochem & Biotechnol, Fac Sci, Chidambaram, Tamil Nadu, India

来源：

HUMAN & EXPERIMENTAL TOXICOLOGY | 2019年 / 38卷 / 07期

关键词：

Mitochondrial enzymes; lysosomal enzymes; cardiac fibrosis; triterpenoid; catecholamine; MATRIX METALLOPROTEINASES; COLORIMETRIC METHOD; TISSUE INHIBITORS; LYSOSOMAL-ENZYMES; CYTOCHROME-C; FIBROSIS; MITOCHONDRIAL; TRANSPORT; APOPTOSIS; DAMAGE;

D O I：

10.1177/0960327119842620

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 ;

摘要：

In the present study, the modulatory effect of ursolic acid (UA) on cardiac fibrosis and mitochondrial and lysosomal enzymes activity in isoproterenol-induced myocardial infarction (MI) in rats were examined. Isoproterenol hydrochloride (ISO; 85 mg/kg body weight) was administered subcutaneously for first two consecutive days. ISO-induced MI in rats significantly decreased the activities of mitochondrial tricarboxylic acid cycle enzymes and respiratory chain enzymes while increased the activities of lysosomal glycohydrolases and cathepsins. The expression of matrix metalloproteinase 2 (MMP-2), MMP-9, collagen type I, alpha-smooth muscle actin (alpha-SMA), and transforming growth factor-beta (TGF-beta) were upregulated in ISO-induced MI in rats. UA administration to rats showed increased activities of mitochondrial tricarboxylic acid cycle enzymes and respiratory chain enzymes and decreased activities of lysosomal glycohydrolases and cathepsins in ISO-induced rats. Furthermore, expression of MMP-2, MMP-9, collagen type I, alpha-SMA, and TGF-beta downregulated in UA-administered rats. Thus, our results demonstrate that UA has an anti-fibrotic effect and attenuates the mitochondrial and lysosomal dysfunction in ISO-induced MI in rats.

引用

页码：785 / 793

页数：9

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