芪苈强心胶囊对心梗后心力衰竭大鼠脂质代谢的影响及作用机制分析

Analysis on Effect of Qili Qiangxin Capsule on Lipid Metabolism in Rats with Heart Failure after Myocardial Infarction and Its Action Mechanism

目的 :分析芪苈强心胶囊对心肌梗死后心力衰竭大鼠脂质代谢的影响及作用机制。方法 :选择60只SD大鼠随机分为空白对照组、模型组、贝那普利组、芪苈强心组,各15只,除空白对照组外均建立心肌梗死后心力衰竭大鼠模型,贝那普利组以10 mg/(kg·d)贝那普利药液灌胃,芪苈强心组以1 g/(kg·d)芪苈强心胶囊药液灌胃,空白对照组、模型组以等体积生理盐水灌胃,8 w后测定各组大鼠血浆3-硝基酪氨酸(3-NT)、8-异前列腺素F_(2α)(8-iso-PGF_(2α))、游离脂肪酸(FFA)水平及心肌组织3-NT蛋白、脂肪酸水平。结果 :(1)模型组、贝那普利组、芪苈强心组血浆3-NT、8-iso-PGF_(2α)、FFA及心肌组织3-NT蛋白水平均高于空白对照组(P <0.05),贝那普利组、芪苈强心组上述指标水平均低于模型组(P <0.05),芪苈强心组上述指标低于贝那普利组(P <0.05);(2)模型组、贝那普利组、芪苈强心组心肌组织n-3系多不饱和脂肪酸(PUFAs)水平均低于空白对照组,n-6系PUFAs水平高于空白对照组(P <0.05),贝那普利组、芪苈强心组心肌组织n-3系PUFAs高于模型组、n-6系PUFAs水平低于模型组(P <0.05),芪苈强心组心肌组织n-3系PUFAs水平高于贝那普利组、n-6系PUFAs水平低于贝那普利组(P <0.05);(3)心力衰竭大鼠血浆FFA水平与C18∶3 n-3、C22∶5 n-3呈负相关(P <0.05),与C18∶2 n-6、C20∶2 n-6、C22∶4 n-6均呈正相关(P <0.05)。结论:芪苈强心胶囊可下调心梗后心力衰竭大鼠血浆3-NT、FFA、8-iso-PGF_(2α)、心肌组织n-6系PUFAs水平,增加n-3系PUFAs水平,提高脂肪酸转运及利用率,改善心肌能量代谢紊乱。

Objective: To analyze the effect of qili qiangxin capsule on lipid metabolism in rats with heart failure after myocardial infarction and its action mechanism. Methods: 60 SD rats were randomly divided into blank control group, model group, benazepril group and qili qiangxin capsule group. 15 rats at each group. Rat models of heart failure after myocardial infarction were established except the blank control group. The rats in the benazepril group were given 10 mg/(kg·d) benazepril by gastric gavage. The rats in the qili qiangxin capsule group were given 1g/(kg·d) qili qiangxin capsule by gastric gavage. The rats in the blank control group and model group were given equal volume of normal saline by gastric gavage. After 8 weeks, the levels of plasma 3-nitrotyrosine(3-NT), 8-isoprostane F2α(8-iso-PGF2α) and free fatty acids (FFA) and the levels of myocardial 3-NT protein and fatty acids were measured. Results: The levels of plasma 3-NT, 8-iso-PGF2α, FFA and myocardial 3-NT protein in the model group, benazepril group and qili qiangxin capsule group were higher than those in the blank control group(P<0.05). The above indexes in the benazepril group and qili qiangxin group were lower than those in the model group(P<0.05), and the above indexes in the qili qiangxin capsule group were lower than those in the benazepril group(P<0.05). The levels of myocardial n-3 polyunsaturated fatty acids(PUFAs) in the model group, benazepril group and qili qiangxin capsule group were lower than those in the blank control group, and the levels of n-6 PUFAs were higher than those in the blank control group(P<0.05). The levels of n-3 PUFAs in the benazepril group and qili qiangxin capsule group were higher than those in the model group, while the levels of n-6 PUFAs were lower than those in the model group(P<0.05). The levels of myocardial n-3 PUFAs in the qili qiangxin capsule group were higher than those in the benazepril group, while the levels of n-6 PUFAs were lower than those in the benazepril group(P<0.05). The levels of plasma FFA in rats with heart failure were negatively correlated with C18∶3 n-3, C22∶5 n-3(P<0.05) and positively correlated with C18∶2 n-6, C20∶2 n-6, C22∶4 n-6(P<0.05). Conclusion: Qili qiangxin capsule can down-regulate levels of plasma 3-NT, FFA, 8-iso-PGF2α and myocardial n-6 PUFAs in rats with heart failure after myocardial infarction, increase the levels of n-3 PUFAs, improve fatty acids’ transport and utilization and improve myocardial energy metabolism disorders.