黄芪甲苷通过AMPK/ACSS2/PPARα信号通路改善心肌细胞能量代谢的机制研究  

Mechanism study of Astragaloside Ⅳ improving energy metabolism of myocardial cells through AMPK/ACSS2/PPARα signaling pathway

作　　者：郭依宁 方崇锴 王俊岩 张璐[1,2,3,4] 方红城[5] 洪晓华 廖蔚茜 冼绍祥[1,2,3,4] 杨忠奇 王陵军[1,2,3,4] 黄育生 GUO Yi-ning;FANG Chong-kai;WANG Jun-yan;ZHANG Lu;FANG Hong-cheng;HONG Xiao-hua;LIAO Wei-qian;XIAN Shao-xiang;YANG Zhong-qi;WANG Ling-jun;HUANG Yu-sheng(The First Affiliated Hospital,Guangzhou University of Chinese Medicine,Guangzhou 510405,China;The First Clinical Medical College of Guangzhou University of Chinese Medicine,Guangzhou 510405,China;Lingnan Medical Research Center,Guangzhou University of Chinese Medicine,Guangzhou 510405,China;Guangdong Provincial Universities Key Laboratory of Chinese Medicine Prevention and Treatment of Chronic Heart Failure,Guangzhou 510405,China;Shenzhen Integrative Medicine Hospital,Shenzhen 518033,China;Huizhou Traditional Chinese Medicine Hospital,Huizhou 516001,China;Traditional Chinese Medicine Hospital of Shenzhen Luohu District,Shenzhen 518021,China)

机构地区：[1]广州中医药大学第一附属医院,广州510405 [2]广州中医药大学第一临床医学院,广州510405 [3]广州中医药大学岭南医学研究中心,广州510405 [4]广东省普通高校慢性心力衰竭中医药防治重点实验室,广州510405 [5]深圳市中西医结合医院,深圳518033 [6]惠州市中医院,惠州516001 [7]深圳市罗湖区中医院,深圳518021

出　　处：《中华中医药杂志》2022年第8期4389-4393,共5页China Journal of Traditional Chinese Medicine and Pharmacy

基　　金：国家自然科学基金项目(No.81973776,No.81973777,No.81804048,No.81673796);广州市科技计划项目(No.202102020123);广州市慢性心力衰竭中医药防治重点实验室项目(No.201705030006)。

摘　　要：目的:探讨黄芪甲苷对血管紧张素Ⅱ(AngⅡ)诱导的HL-1心肌细胞肥大的作用机制。方法:将HL-1心肌细胞分为空白组,AngⅡ组,黄芪甲苷低、中、高剂量组,共同培养24 h。收集各组细胞,CCK8检测细胞活性,检测细胞ATP含量,免疫荧光检测细胞ACSS2的表达情况,RT-PCR、Western Blot检测细胞心肌肥大相关指标mRNA及蛋白表达情况。结果:与AngⅡ组比较,黄芪甲苷各剂量组细胞活力显著增加(P<0.01),细胞内ATP含量显著升高(P<0.01),ANP、BNP、Myh7 mRNA及蛋白表达水平降低(P<0.01),AMPK、ACSS2、PPARαmRNA水平显著升高(P<0.01),p-AMPK/AMPK、ACSS2、PPARα、PGC-1α蛋白表达显著增加(P<0.01)。结论:黄芪甲苷可以抑制AngⅡ诱导的心肌细胞肥大,改善心肌细胞能量代谢,其机制可能与激活AMPK/ACSS2/PPARα信号通路有关。Objective:The study mainly discussed the effect of Astragaloside Ⅳ(AS-Ⅳ) on HL-1 cardiomyocytes induced by angiotensin Ⅱ(AngⅡ) and explored the possible mechanisms.Methods:The experiment was divided into control group,AngⅡgroup,astragaloside Ⅳ low,medium,and high dose groups.The cell viability and intracellular ATP concentration were tested in each group after being cultured for 24 hours.The expression of ACSS2 in each group was detected by Immunofluorescence.The expression of myocardial hypertrophy markers were detected by RT-PCR and Western Blot.Results:Compared with the AngⅡgroup,the cell viability and ATP contents were significantly increased(P<0.01).The expression of AMPK,ACSS2,PPARα mRNA were increased and the protein expression levels of p-AMPK/AMPK,ACSS2,PPARα,and PGC-1α were increased significantly in AS-Ⅳ groups while the mRNA and protein levels of ANP,BNP,Myh7 were significantly reduced(P<0.01).Conclusion:AS-Ⅳ can inhibit cardiomyocyte hypertrophy induced by AngⅡ,and improve energy metabolism on HL-1 cell,and its mechanism may be associated with the activation of AMPK/ACSS2/PPARα signaling pathway.

关 键 词：黄芪甲苷 心肌细胞 血管紧张素Ⅱ 乙酰辅酶A合成酶2 能量代谢 

分 类 号：R285.5[医药卫生—中药学]