Long-term oral Asperosaponin VI attenuates cardiac dysfunction, myocardial fibrosis in a rat model of chronic myocardial infarction

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• 作者：Chunmei Li^a ; Yonglin Gao^b ; ^{gylbill@163.com} ; ^{sdlcm1978@163.com} ; Jingwei Tian^a ; ; Yanli Xing^c ; Haibo Zhu^c ; Jingyu Shen^b
• 关键词：ASA VI ; Asperosaponin VI ; CHF ; congestive heart failure ; ECG ; electrocardiogram ; GSH-Px ; glutathione peroxidase ; HR ; heart rate ; IS ; infarct size ; IL-6 ; interleukin 6 ; LAD ; left anterior descending ; LV ; left ventricular ; LVEDP ; left ventricular end-diasto
• 刊名：Food and Chemical Toxicology
• 出版年：2012
• 期刊代码：20_02786915
• 类别：pha
• 出版时间：May, 2012
• 卷：50
• 期：5
• 页码：1432-1438
• 文件大小：1269 K

摘要

The aim of the study was to determine the effects of Asperosaponin VI (ASA VI), a triterpene saponin isolated from Dipsacus asper Wall, on chronic myocardial infarction (MI) and possible mechanisms in rats. MI was induced by permanent ligation of the left coronary artery. Twenty-four hours after MI, the rats were administered the extract by gavage (once a day). Six weeks after MI/sham surgery, cardiac dysfunction, infarct size (IS), cardiac fibrosis, hydroxyproline concentration, the oxidative stress parameter and inflammation mediators were examined. The results indicated that ASA VI improved left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), 卤dP/dt, heart weight/body weight, right ventricular weight/body weight and lung weight/body weight (P < 0.01, P < 0.05). These were accompanied by the attenuation of cardiac fibrosis, IS and hydroxyproline concentration (P < 0.01, P < 0.05). ASA VI could decrease the levels of tumor necrosis factor-伪 (TNF-伪) and interleukin 6 (IL-6), but increase IL-10 content (P < 0.01, P < 0.05). Furthermore, it also could raise the activities of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), but reduce malonyldialdehyde (MDA) level (P < 0.01, P < 0.05). The results indicated that ASA VI improved cardiac function and myocardial fibrosis from myocardial ischemia injury, and this cardioprotection might be attributed to reduce oxidative stress and regulate inflammation mediators.