黄芪多糖对腹主动脉缩窄致大鼠心肌肥厚能量代谢紊乱的抑制作用

Inhibitory effect of Astragalus polysaccharide on energy metabolism of myocardia hypertrophy induced by abdominal aorta constriction in rats

目的探讨黄芪多糖(APS)对腹主动脉缩窄(AAC)致大鼠心肌肥厚的抑制作用及其机制。方法大鼠采用结扎腹主动脉的方法制备AAC模型,1周后ig给予大鼠APS 200,400和800 mg.kg-1,每天1次,共11周。计算心脏质量指数(HMI)和左心室质量指数(LVMI);测定左心室收缩压(LVSP)、左心室舒张末压(LVEDP)和左心室内压最大升降速率(±dp/dtmax),HE染色观察大鼠左室心肌形态学改变;测定左心室乳酸(LAC)、游离脂肪酸(FFA)含量;采用逆转录-聚合酶链反应(RT-PCR)测定心肌心钠素mRNA(ANPmRNA)表达;测定心肌细胞线粒体膜电位(MMP)。结果与假手术组相比,AAC模型组的大鼠,MMP明显降低,其他指标均显著增高。与模型组相比,APS 800 mg.kg-1组HMI,LVMI,LVSP,LVEDP和±dp/dtmax均显著降低(P<0.05);APS 400和800 mg.kg-1组ANP mRNA表达明显下降,MMP明显升高(P<0.05);APS200,400和800 mg.kg-1组LAC水平明显降低(<0.05)。结论 APS能够有效抑制AAC大鼠心肌肥厚并改善其能量代谢紊乱,提高线粒体的活力。

OBJECTIVE To explore the effect of Astragalus polysaccharide（APS） on hypertrophic myocardium caused by abdominal aorta constriction in rats,and to explore its molecular mechanism.METHODS Myocardial hypertrophy model in rats was established by adopting abdominal aorta constriction（AAC）.APS 200,400 and 800 mg·kg-1 were ig given to the rats for 11 weeks.Heart mass index（HMI）and left ventricular mass index（LVMI） were detected.Left ventricular systolic pressure（LVSP）,left ventricular end-diastolic pressure（LVEDP）,and maximum rate of rise/decrease of LVSP（±dp/dtmax） were detected,and pathological section by HE staining.Lactic acid（LAC） and free fatty acids（FFA） were measured.mRNA expression of heart atrial natriuretic peptide（ANP） was observed by RT-RCR.The mitochondrial membrane potential（MMP） was measured.RESULTS Compared with sham group,MMP significantly decreased and other indicators significantly elevated in all index in AAC group.Compared with AAC group,APS 800 mg·kg-1 decreased HMI,LVMI,LVSP,LVEDP and ±dp/dtmax（P0.05）.APS 400 and 800 mg·kg-1 could also remarkably down-regualte the overexpressions of ANP mRNA induced by AAC and significantly improved MMP level（P0.05）.LAC content effectively decreased by APS 200,400 and 800 mg·kg-1（P0.05）.CONCLUSION APS significantly improves myocardial energy metabolism in AAC rats and protects the function of myocardial mitochondria.