养心康片通过(Akt/AMPK)-mTOR通路抑制心梗后心力衰竭模型兔心肌细胞凋亡的机制

任培华; 王鹏; 廖东江; 李振球; 朱汉平; 胡素珍

doi:10.13422/j.cnki.syfjx.20181533

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养心康片通过(Akt/AMPK)-mTOR通路抑制心梗后心力衰竭模型兔心肌细胞凋亡的机制

药理 | 更新时间：2024-01-04

- 养心康片通过(Akt/AMPK)-mTOR通路抑制心梗后心力衰竭模型兔心肌细胞凋亡的机制
- Mechanism of Yangxinkang Tablet in Inhibiting Cardiomyocyte Apoptosis in Rabbit with Heart Failure After Myocardial Infarction Through Akt/AMPK-mTOR Pathway
- 中国实验方剂学杂志 2018年24卷第16期页码：124-130
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家自然科学基金面上项目（81673902）;广州市教育局项目（1201411088）;广东省中医药局项目（20142093）
- DOI：10.13422/j.cnki.syfjx.20181533
  中图分类号： R-332;R285.5
- 纸质出版日期：2018
- 稿件说明：
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任培华, 王鹏, 廖东江, 等. 养心康片通过(Akt/AMPK)-mTOR通路抑制心梗后心力衰竭模型兔心肌细胞凋亡的机制[J]. 中国实验方剂学杂志, 2018,24(16):124-130.

REN Pei-hua, WANG Peng, LIAO Dong-jiang, et al. Mechanism of Yangxinkang Tablet in Inhibiting Cardiomyocyte Apoptosis in Rabbit with Heart Failure After Myocardial Infarction Through Akt/AMPK-mTOR Pathway[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(16): 124-130.
任培华, 王鹏, 廖东江, 等. 养心康片通过(Akt/AMPK)-mTOR通路抑制心梗后心力衰竭模型兔心肌细胞凋亡的机制[J]. 中国实验方剂学杂志, 2018,24(16):124-130. DOI： 10.13422/j.cnki.syfjx.20181533.

REN Pei-hua, WANG Peng, LIAO Dong-jiang, et al. Mechanism of Yangxinkang Tablet in Inhibiting Cardiomyocyte Apoptosis in Rabbit with Heart Failure After Myocardial Infarction Through Akt/AMPK-mTOR Pathway[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(16): 124-130. DOI： 10.13422/j.cnki.syfjx.20181533.

摘要

目的：观察养心康片通过[蛋白激酶B（protein kinase B，Akt）/腺苷酸活化蛋白激酶（AMP-activated kinase，AMPK）]-乳动物雷帕霉素靶蛋白（mammalian target of rapamycin，mTOR）通路对心梗后心力衰竭模型兔心肌细胞凋亡的影响。方法：应用结扎冠脉的方法建立心梗后心力衰竭兔模型，随机分为模型组，养心康组，AMPK抑制剂组（10 mg·kg-1 Compound C腹腔注射，每日2次），Akt抑制剂组（10 mg·kg-1 casodex灌胃，每日2次）和mTOR抑制剂组（0.5 mg·kg-1 rapamycin灌胃，每日2次），并设立正常组，每组5只，共30只。给予养心康片0.51 g·kg-1 灌胃，每日1次，正常组和模型组给予等体积的蒸馏水灌胃，共4周。心脏彩超检测心功能，蛋白免疫印迹法（Western blot）检测心肌B细胞淋巴瘤/白血病-2（Bcl-2），Bcl-2相关X蛋白（Bax）蛋白表达，原位末端凋亡法（TUNEL）检测心肌细胞凋亡。结果：与正常组比较，模型组的左室射血分数（LVEF）值降低（P<0.01），Bcl-2，Bax蛋白表达量增高（P<0.05，P<0.01），Bcl-2/Bax降低（P<0.01），心肌细胞凋亡率升高（P<0.01）；与模型组比较，养心康组的LVEF值升高（P<0.01），Bax蛋白表达量降低（P<0.01），Bcl-2/Bax升高（P<0.01），心肌细胞凋亡率降低（P<0.01）。与抑制剂各组比较，养心康组的LVEF值升高（P<0.01），Bcl-2/Bax升高（P<0.01），心肌细胞凋亡率降低（P<0.01）。结论：养心康片可通过干预（Akt/AMPK）-mTOR通路调控心肌细胞Bcl-2，Bax蛋白表达水平减少心肌细胞凋亡，改善心梗后心衰模型的心脏功能。

Abstract

Objective: To observe the effect of Yangxinkang tablet on cardiomyocyte apoptosis in rabbit with heart failure after myocardial infarction through protein kinase B (Akt)/AMP-activated kinase (AMPK)-the mammalian target of rapamycin (mTOR) pathway. Method: The rabbit model of heart failure was established through ligation of coronary artery. A total of 30 experimental animals were randomly divided into model group

Yangxinkang group

AMPK inhibitor group (10 mg·kg-1 Compound C

intraperitoneal injection

2 times a day)

Akt inhibitor group (10 mg·kg-1 casodex

intragastric administration

2 times a day) and mTOR inhibitor group (0.5 mg·kg-1 rapamycin

intragastric administration

2 times a day)

and a blank control group was also set up

with 5 in each group. Yangxinkang tablet (0.51 g·kg-1) were intragastrically administered once a day. Blank control group and experimental groups were given the equivalent volume of distilled water for 4 weeks. Heart function was detected by color Doppler ultrasound

Bcl-2 and Bax protein expressions were detected by Western blot

and cardiomyocyte apoptosis was detected by TdT-mediated DUTP nick end labeling(TUNEL). Result: Compared with the blank control group

the LVEF value of the model group decreased (P<0.01)

the expressions of Bcl-2 and Bax protein increased (P<0.05

P<0.01)

the Bcl-2/Bax ratio decreased (P<0.01)

and cardiomyocyte apoptosis rate was increased (P<0.01). Compared with the model group

the LVEF value of the Yangxinkang group was increased (P<0.01)

the expression of Bax protein was decreased (P<0.01)

the Bcl-2/Bax ratio was increased (P<0.01)

and the cardiomyocyte apoptosis rate was decreased (P<0.01). Compared with each inhibitor groups

the LVEF value of Yangxinkang group was increased (P<0.01)

Bcl-2/Bax ratio was increased (P<0.01)

and the cardiomyocyte apoptosis rate was decreased (P<0.01). Conclusion: Yangxinkang tablet can regulate the expressions of Bcl-2 and Bax protein in cardiac myocytes

reduce cardiomyocyte apoptosis through Akt/AMPK-mTOR pathway and improve the cardiac function of heart failure model after myocardial infarction.

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