Effects of Jia-Shen Prescription on Cardiac Function and Cytokine Production in Early Phase of Myocardial Infarction in Rats / 世界科学技术-中医药现代化

ABSTRACT

This article was aimed to determine effects of Jia-Shen prescription (JSP) on infarct size (IS), cardiac function and myocardial cytokine in the early phase of myocardial infarction (MI) in rats. Acute MI models were induced by the ligation of left anterior descending coronary artery in Sprague-Dawley (SD) rats. The rats were ran-domly divided into five groups, which were the sham-operated group, model group, JSP-3 g (3 g·kg-1·day-1) group, JSP-6 g (6 g·kg-1·day-1) group, and the losartan (10 mg·kg-1·day-1) group. IS was determined by Evans blue and 2,3,5-Triphenyltetrazolium chloride (TTC) 3 days after MI. The left ventricular structure and contractility were measured by echocardiography performed 7 days after MI. And contents of myocardial inflammatory mediators in-cluding tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and monocyte chemoattractant protein-1 (MCP-1) were measured by ELISA. The results showed that compared with the model group, treatment with JSP at the dose of 6 g significantly reduced myocardial IS (P<0.05);left ventricular end diastolic diameter (LVEDD) and left ventricu-lar end systolic diameter (LVESD) were significantly decreased (P<0.05); left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) were significantly increased (P<0.05).The results were similar as the losartan group. Compared with the model group, JSP can significantly reduce the production of TNF-α, IL-1βand MCP-1 in cardiac tissues (P<0.05). Except TNF-α, these effects of JSP were in a dose-dependent manner. JSP (6 g) had equal effectiveness with losartan. It was concluded that consistent with losartan-induced cardioprotection, JSP administered after MI reduced myocardial IS, improved cardiac function, and decreased inflammatory mediators in ischemic myocardium. The data indicated that JSP exerted its cardioprotection possibly via inhibiting inflammatory response.