ABSTRACT
This study was aimed to observe the effect ofJia-Shen prescription (JSP) on angiotensinⅡ (AngⅡ) inhibition, ventricular remodeling in myocardial infarction (MI) rat model. The anterior descending coronary artery of Sprague-Dawley rat was ligated to establish the MI rat model. Rats were randomly divided into the 3 g JSP group, 6 g JSP group, losartan group, model group, and the sham-operation group. Intragastric administration of medication was given 24 h after MI. In the 3 g and 6 g JSP group, JSP was given at the dose of 3 g·kg-1·day-1 and 6 g·kg-1day-1, respectively. Losartan was given at the dose of 10 mg·kg-1·day-1 in the losartan group. Same volume of distilled water was given to the sham-operation and model group. Four weeks later, the left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD), posterior wall thickness (PWT), left ventricular ejection fraction (LVEF), left ventricular fractional shorten (LVFS), left ventricular weight index (LVWI), the distribution and content of collagen, plasma brain natriuretic peptide (BNP) and the AngⅡ content in myocardial tissues homogenate were observed. The results showed that 4 weeks after MI, compared to the model group, 6 g PJP reduced myocardial infarct size, LVWI, LVEDD and LVESD, and enhanced LVEF and LVFS (P< 0.05). In ischemic regions, compared to the model group, JSP can obviously reduce the content of collagen (P < 0.05). This effect had dose-dependent relationship. Plasma BNP and AngⅡ content in myocardial tissues homogenate were also obviously lower than the model group (P< 0.05). It was concluded that JSP can improve the ventricular remodeling of MI rat model. Its action mechanism may be through the AngⅡ inhibition, in order to improve the early stage left ventricular morphological remodeling, myocardial fibrosis and cardiac contractile function.
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.
