三七总皂苷对心梗后心室重构大鼠增强抗氧化与改善心肌形态学作用

Effects of Panax Notoginsenoside on Potentiating Antioxidation and Improving Myocardial Morphology in Rats with Post-myocardial Infarction-ventricular Remodeling

为研究三七总皂苷（PNS）对急性心肌梗塞（AMI）后左室重构（LVRM）大鼠自由基损伤和心肌细胞形态学改变的作用，采用结扎大鼠左冠状动脉前降支的方法，建立AMI模型，术后24h后随机分为对照组和实验组，连续4周分别灌胃给予生理盐水和PNS低、中、高剂量，观察PNS和福辛普利对病鼠血清丙二醛（MDA）、c反应蛋白（CRP）、肌红蛋白-I（cTn—I）及肌酸激酶同工酶（CK—MB）、谷胱甘肽过氧化物酶（GSH—Px）、一氧化氮（NO）及心肌细胞形态病理结构和心脏指数改变等的影响。结果发现与对照组比较，PNS与福辛普利均能显著改善病鼠左室心肌细胞形态结构病理改变及心脏指数（P〈0．01），显著降低MDA、CRP、CK—MB与cTn—I、提高GSH—Px活性（P〈0．01—0．05），高剂量PNS可明显降低NO含量（P〈0．05）。可见PNS可通过抑制脂质过氧化反应，减轻病鼠心肌细胞的病理损伤，增强抗氧化，具有抑制心肌肥大与改善心室重构心肌细胞形态学结构作用。

It was studied the Panax Notoginsenoside （PNS） on free radical injury and cardiac myocytes＇ morphological alterations in rats with acute post-myocardial infarction （AMI） left ventricular remodeling （LVRM）. By ligation in rats left anterior descending coronary artery, building rat model of AMI, after 24 hours of postoperative, the rats were randomly divided into control and experimental groups, then respectively gavaged NS and the low,middle and high dosage of PNS for four consecutive weeks to observe the index such as Malondialdehyde （ MDA）,C-reactive protein （CRP）, Troponin-I （cTn-I）, Creatine kinase isoenzymes （CK-MB）, Glutathione peroxidase （GSH-PX）, Nitric oxide （NO） and the pathological structure of cardiac myocytes, cardiac index of PNS and Fosinopril in the disease rats. The result showed that compared with the NS group, PNS and Fosinopril can be significandy improved pathological changes and cardiac index of left ventricular cardiac myocytes＇ morphology rats （P 〈0. 01 ）, the biochemistry index SOD, MDA, CRP, CK-MB and cTn-I are all significantly lower, the activity of GSH-PX significantly enhanced （P 〈0. 01 -0.05）, the high-dose PNS group can decrease NO （P 〈0. 05）. So,through, inhibiting lipid peroxidation in rats, PNS can reduce pathological injury of cardiac myocytes, enhance the antioxidance, inhibit cardiac hypertrophy and improve ventricular remodeling, morphological structure of cardiacmyocytes in post AMI LVRM rats.