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目的观察熊果酸对小鼠急性心肌梗死的作用及机制。方法通过结扎小鼠冠状动脉左前降支构建急性心肌梗死模型。将50只雄性C57小鼠随机分成假手术组、梗死模型组和熊果酸低、中、高3个剂量组。梗死模型组和熊果酸组结扎冠状动脉左前降支24h,假手术组操作同上,但不夹闭左冠状动脉。熊果酸组在术前4h分别给予熊果酸4、8、12mg·kg~(-1)腹腔注射。假手术组和梗死模型组同时给予等体积生理氯化钠注射液腹腔注射。观察熊果酸对小鼠心肌梗死面积,心肌病理形态改变,血清乳酸脱氢酶(LDH),磷酸肌酸激酶(CPK),丙二醛(MDA),过氧化氢酶(CAT),谷胱甘肽过氧化物酶(GPx),超氧化物歧化酶(SOD),脂质过氧化物(LPO),血浆6-酮-前列腺素F1α(PGI_2)及血栓素B_2(TXA_2)水平,以及心肌梗死区和非梗死区游离脂肪酸(FFA)含量的影响。结果熊果酸预处理可减少心肌梗死面积和心肌病理形态改变,下调血清中LDH、CPK、LPO、MDA含量以及血浆中TXA_2和心肌梗死区和非梗死区FFA含量,增加血清中CAT和GPx以及血浆中PGI2含量。结论熊果酸对急性心肌梗死小鼠心肌具有明显的保护作用,其机制可能与减轻氧化损伤和脂质代谢紊乱相关。
Objective To observe the effect and mechanism of ursolic acid on acute myocardial infarction in mice. Methods Acute myocardial infarction model was established by ligation of the left anterior descending coronary artery in mice. Fifty male C57 mice were randomly divided into sham operation group, infarction model group and ursolic acid low, medium and high dose groups. The infarct model group and ursolic acid group ligation of the left anterior descending coronary artery 24h, sham-operated group operation above, but not the left coronary artery. The ursolic acid group was administered intraperitoneally with 4, 8 and 12 mg · kg -1 of ursolic acid at 4 hours before operation. Sham operation group and infarction model group were given equal volume of physiological sodium chloride injection intraperitoneal injection. To observe the effect of ursolic acid on myocardial infarct size, myocardial pathomorphology, serum LDH, CPK, MDA, catalase (CAT), glutathione (GPx), superoxide dismutase (SOD), lipid peroxide (LPO), plasma 6-keto-prostaglandin F1α (PGI_2) and thromboxane B_2 (TXA_2) Effect of Free Fatty Acids (FFA) on Infarct and Non-infarct Zone. Results Ursolic acid preconditioning can reduce myocardial infarct size and myocardial pathomorphology, decrease serum levels of LDH, CPK, LPO and MDA, as well as TXA 2 in plasma and FFA content in myocardial infarction and non-infarction areas, increase CAT and GPx levels in serum Plasma PGI2 content. Conclusion Ursolic acid has a significant protective effect on myocardium of acute myocardial infarction mice, and its mechanism may be related to reducing oxidative damage and lipid metabolism disorders.