AMPK/p38 MAPK通路介导黄芪多糖抑制大鼠心肌肥厚的研究  

AMPK/p38 MAPK pathway mediates astragalus polysaccharides in inhibiting myocardial hypertrophy in rats

作　　者：陈广琴[1] 何金龙 曲楠[1] 白法文 洪钰杰 蓝金 Chen Guangqin;He Jinlong;Qu Nan;Bai Fawen;Hong Yujie;Lan Jin(Department of Cardiology,Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine,Nanning 530000,China)

机构地区：[1]广西中医药大学附属瑞康医院心内科,南宁530000

出　　处：《广西医科大学学报》2020年第6期1018-1023,共6页Journal of Guangxi Medical University

基　　金：国家自然科学基金资助项目(No.81660776);2017年度广西中青年基础能力提升资助项目(No.2017KY0296)。

摘　　要：目的:探讨黄芪多糖(APS)对心肌肥厚大鼠心肌组织AMPK/p38 MAPK通路的影响。方法:健康SD大鼠60只,雌雄各30只,随机分为5组:模型组,APS低、中、高剂量(L-APS、M-APS、H-APS)组,假手术组。模型组及L-APS、M-APS、H-APS组通过开腹结扎腹主动脉的方法构造心肌肥厚大鼠模型。术后1周开始,给予相应药物干预:L-APS、M-APS、H-APS组分别灌胃给予APS 200 mg·kg/d^-1、400 mg·kg/d^-1、800 mg·kg/d^-1,假手术组及模型组则给予同等体积蒸馏水灌胃。8周后,测定大鼠心肌重量指数(HMI)、左室重量指数(LVMI);应用苏木精-伊红(HE)染色观察心肌细胞形态并测定心肌细胞直径和表面积;Western blotting分别检测心肌组织AMPK、p38 MAPK的蛋白表达量。结果:模型组大鼠HMI、LVMI、心肌细胞直径和表面积均较假手术组增加(P<0.01),心肌明显肥厚;与模型组相比,APS各剂量组HMI、LVMI、心肌细胞直径和表面积均有不同程度降低,以H-APS组最为显著(P<0.01);H-APS组心肌无明显肥厚;APS各剂量组AMPK、p38MAPK磷酸化表达水平较模型组上调,以H-APS组明显(P<0.01)。结论:APS能改善主动脉缩窄所致的大鼠心肌肥厚,AMPK/p38 MAPK通路可能介导了APS抑制心肌肥厚的保护作用。Objective:To explore the effect of astragalus polysaccharides(APS)on the AMPK/p38 MAPK pathway in myocardial tissues of rats with myocardial hypertrophy.Methods:60 healthy SD rats,30 males and 30 males,were randomly divided into 5 groups:model group,APS low,medium and high dose(L-APS,M-APS,HAPS)groups,and sham operation group.The model group,L-APS,M-APS,and H-APS groupsweregivenabdominal aorta ligationto establishthe myocardial hypertrophy rat model.After one week of operation,the corresponding drug intervention was given:L-APS,M-APS,H-APS groups were given APS at 200 mg/kg/day,400 mg/kg/day,and 800 mg/kg/dayby intragastric administration respectively,and the sham operation group and model group were given the same volume of distilled waterbyintragastric administration.After 8 weeks,the heart mass index(HMI)and left ventricular mass index(LVMI)of rats were measured.Hematoxylin-eosin(HE)staining was used to observe the morphology of myocardial cells and measure the diameter and surface area of myocardial cells.Western blotting was used to detect the protein expression levels of AMPK and p38 MAPK in the myocardial tissues.Results:The HMI,LVMI,myocardial cell diameter,and surface area of the model group were increased thanthose of the sham operation group(P<0.01),and the myocardium was significantly hypertrophicof the model group.Compared with the model group,the HMI,LVMI,myocardial cell diameter,and surface area of the all APS groups were decreased to different degrees,especiallyin the H-APS group(P<0.01).The myocardium of the H-APS group had no significant hypertrophy.The expression levels of AMPK andp38 MAPK phosphorylation in all APS group were up-regulated than those in the model group,especially in the H-APS group(P<0.01).Conclusion:APS can improve myocardial hypertrophy induced by aortic constriction.AMPK/p38 MAPK pathway may mediate the protective effect of APS on myocardial hypertrophy.

关 键 词：黄芪多糖 主动脉缩窄 心肌肥厚 AMPK/p38 MAPK信号通路 

分 类 号：R542.23[医药卫生—心血管疾病]