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Effect of Yuxingeng Fluid on Myocardial Energy Metabolism in Wistar Rats with Acute Myocardial Infarction

机译:鱼腥eng液对Wistar大鼠急性心肌梗死心肌能量代谢的影响

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Objective: To examine the effect of Yuxingeng fluid (YXGF) on myocardial energy metabolism in Wistar rats with acute myocardial infarction (AMI) by observing the ultrastructure of mitochondria and the enzyme activities of rat myocardial adenosine triphosphate (ATP), succinate dehydrogenase (SDH), acid phosphatase (ACP), alkaline phosphatase (ALP) and the content of glycogen. Methods: AMI models were established by ligature of left anterior descending coronary artery and then the rats with AMI were randomly divided into 7 groups: namely, blank group, model group, sham-operated group, captopil group, high-dose YXGF group, middle-dose YXGF group and low-dose YXGF group. From the next day after modeling, the rats were given YXGF through gastrogavage which lasted for 4 weeks. And then, the ultra-structure of mitochondria was observed by electronic microscope and the enzyme activities of ATP, SDH, ACP, ALP and the content of glycogen were determined. Results: Compared with model group, the other three groups of high-dose YXGF, middle-dose YXGF, low-dose YXGF and captopril group could protect the ultrastructure of mitochondria and significantly increase enzyme activities of ATP, SDH, ACP, ALP and the content of glycogen (P<0.01). Conclusion: YXGF can protect mitochondria and increase myocardial enzyme activities and the content of glycogen, which may be one of the mechanisms intervening in the pathological course of the early ventricular remodeling in rats with AMI.
机译:目的:观察鱼腥eng液(YXGF)对Wistar大鼠急性心肌梗死(AMI)心肌能量代谢的影响,观察其线粒体的超微结构以及大鼠心肌三磷酸腺苷(ATP),琥珀酸脱氢酶(SDH)的酶活性。 ,酸性磷酸酶(ACP),碱性磷酸酶(ALP)和糖原含量。方法:结扎左冠状动脉前降支建立AMI模型,然后将AMI大鼠随机分为7组:空白组,模型组,假手术组,卡托吡尔组,大剂量YXGF组,中度大剂量YXGF组和小剂量YXGF组。从建模后的第二天开始,通过胃管灌胃给予大鼠YXGF,持续4周。然后,通过电子显微镜观察线粒体的超微结构,并测定ATP,SDH,ACP,ALP的酶活性和糖原含量。结果:与模型组相比,高剂量YXGF,中剂量YXGF,低剂量YXGF和卡托普利组的其他三组均能保护线粒体的超微结构,并显着增加ATP,SDH,ACP,ALP和ATP酶的活性。糖原含量(P <0.01)。结论:YXGF可以保护线粒体,增加心肌酶活性和糖原含量,可能是干预AMI大鼠早期心室重构的病理机制之一。

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