基于PI3K通路探讨参芪苈心方对心肌细胞的保护作用  

Protective effects of Shenqi Lixin formual on cardiomyocytes based on PI3K pathway

作　　者：李晨 梁凡 胡明旭 隋艳波[1] LI Chen;LIANG Fan;HU Mingxu;SUI Yanbo(First Affilliated Hospital,Heilongjiang University of Chinese Medicine,Harbin 150000,China;Heilongjiang Academy of Traditional Chinese Medicine,Harbin 150080,China)

机构地区：[1]黑龙江中医药大学附属第一医院,黑龙江哈尔滨150000 [2]黑龙江省中医药科学院,黑龙江哈尔滨150080

出　　处：《陕西中医》2025年第3期291-295,共5页Shaanxi Journal of Traditional Chinese Medicine

基　　金：国家自然科学基金青年基金资助项目(81904107);黑龙江省自然科学基金资助项目(LH2022H071)。

摘　　要：目的:探讨参芪苈心方调节磷脂酰肌醇-3-激酶(PI3K)/蛋白激酶B(Akt)通路,抑制血管紧张素Ⅱ(AngⅡ)诱导H9c2细胞凋亡的作用和机制。方法:制备参芪苈心方含药血清,AngⅡ诱导H9c2细胞损伤,分为空白组、模型组、含药血清高、中、低剂量组、卡托普利组。流式细胞仪检测细胞凋亡,Western blotting法、免疫组化技术检测H9c2细胞色素C(Cyt-C)、Bcl-2相关X蛋白(Bax)、B淋巴细胞瘤-2(Bcl-2)、半胱氨酸天冬氨酸特异性蛋白酶-9(Caspase-9)、PI3K、Akt、p-Akt蛋白表达水平,检测线粒体膜电位(MMP)。结果:参芪苈心方含药血清能提高H9c2细胞活力与MMP表达。与模型组相比,参芪苈心方含药血清组中PI3K、Bcl-2表达明显增加,MMP升高,Bax、Cyt-C、Caspase-9表达下降(P<0.05),且与剂量呈正相关。PI3K信号通路阻断剂LY29400干预后,高剂量组p-Akt表达降低,但Akt表达在各组间比较,差异无统计学意义(P>0.05)。结论:参芪苈心方含药血清可抑制AngⅡ诱导心肌细胞凋亡。通过调节PI3K/Akt信号通路,提高Bcl-2水平,降低Bax、Caspase-9表达,增加细胞活力,抑制细胞凋亡线粒体途径,发挥心肌细胞保护作用。Objective:To investigate role and mechanism of angiotensinⅡ(AngⅡ)-induced apoptosis in H9c2 cells by regulating phosphatidylinositol-3-kinase(PI3K)/protein kinase B(Akt)pathway.Methods:AngⅡinduced H9c2 cell damage,divided into blank group,model group,high,medium and low dose group of medicated serum,captopril group.Apoptosis was detected by flow cytometry,expression levels of H9c2 cytochrome C(Cyt-C),Bcl-2-related X protein(Bax),B lymphocytoma-2(Bcl-2),cysteine aspartate-specific protease-9(Caspase-9),PI3K,Akt and p-Akt proteins were detected by Western blotting and immunohistochemistry.The expression of mitochondrial membrane potential(MMP)was detected.Results:The medicated serum of Shenqi Lixin formual could significantly increase viability and MMP expression of H9c2 cells.Compared with the model group,the expression levels of PI3K,Bcl-2,MMP increased,and the expression levels of Bax,Cyt-C and Caspase-9 were significantly decreased in the Shenqi Lixin formual group(P<0.05),which was positively correlated with the dose.There was no significant difference in the expression of Akt between the groups after LY29400 intervention with PI3K signaling pathway blocker(P>0.05).The expression of p-Akt in the high-dose Shenqi Lixin formual group were significantly reduced.Conclusion:The medicated serum of Shenqi Lixin formual can inhibit apoptosis of cardiomyocytes induced by AngⅡ.It may increase the level of Bcl-2 and reduce expression of Bax and Caspase-9 by regulating the PI3K/Akt signaling pathway,thereby increasing cell viability,inhibiting apoptotic mitochondrial pathway,and exerting cardiomyocyte protection.

关 键 词：心力衰竭 参芪苈心方 磷脂酰肌醇-3-激酶 蛋白激酶B 细胞凋亡 心肌细胞 AngⅡ 

分 类 号：R289[医药卫生—方剂学]