| 赵彩霞,刘建芳,刘宏,李军,刘爽,庞鑫鑫,谷彦玲.雷公藤甲素对心力衰竭大鼠心肌损伤及AMPK/mTOR通路的影响.[J].中南医学科学杂志.,2025,(1):23-27, 69. |
| 雷公藤甲素对心力衰竭大鼠心肌损伤及AMPK/mTOR通路的影响 |
| Effects of triptolide on myocardial injury and AMPK/mTOR pathway in heart failure rats |
| 投稿时间：2023-09-24 修订日期：2024-10-12 |
| DOI：10.15972/j.cnki.43-1509/r.2025.01.005 |
| 中文关键词: 雷公藤甲素 心力衰竭 心肌损伤 腺苷酸活化蛋白激酶/哺乳动物雷帕霉素靶蛋白通路 大鼠 [ |
| 英文关键词:triptolide heart failure myocardial injury AMPK/mTOR rats |
| 基金项目:河北省中医药管理局科研课题(2022442) |
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| 中文摘要: |
| 目的探究雷公藤甲素(TP)对心力衰竭(HF)大鼠心肌损伤及腺苷酸活化蛋白激酶(AMPK)/哺乳动物雷帕霉素靶蛋白(mTOR)通路的影响。 方法将60只SPF级SD雄性大鼠随机均分为假手术组(Sham组)、模型组(Model组)、低剂量TP组(TP-L组,100 μg/kg TP)、高剂量TP组(TP-H组,200 μg/kg TP)和高剂量TP+AMPK抑制剂Compound C组(TP-H+CC组,200 μg/kg TP+0.2 mg/kg Compound C)。除Sham组外,其余组大鼠通过结扎冠状动脉左前降支构建HF模型。采用超声心动图检测各组大鼠心功能指标；采用HE、TUNEL染色法分别检测大鼠心肌组织病理学变化、心肌细胞凋亡情况；ELISA检测大鼠心肌组织脑钠肽、心肌肌钙蛋白Ⅰ、肿瘤坏死因子-α、白细胞介素-6水平以及血清丙二醛、超氧化物歧化酶水平。Western blotting法测定心肌AMPK/mTOR信号通路及凋亡标志蛋白表达水平。 结果HF大鼠心功能下降、心肌细胞凋亡率增加,心肌组织细胞排列紊乱,间隙变宽,心室壁变薄,出现大量炎症细胞浸润和氧化应激反应；AMPK/mTOR信号通路被抑制。高剂量TP干预后,HF大鼠心功能得到提高；心肌细胞凋亡、炎症反应和氧化应激得以改善,AMPK/mTOR信号通路激活；而AMPK抑制剂Compound C减弱了TP对HF大鼠心肌损伤的改善。 结论TP可能通过激活AMPK/mTOR信号通路减轻HF大鼠的心肌损伤。 |
| 英文摘要: |
| AimTo investigate the effects of triptolide (TP) on myocardial injury and the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway in heart failure (HF) rats. Methods60 SPF grade SD male rats were randomly divided into sham surgery group (Sham group), Model group, low-dose TP group (TP-L group, 100 μg/kg TP), high-dose TP group (TP-H group, 200 μg/kg TP), and high-dose TP+AMPK inhibitor Compound C group (TP-H+CC group, 200 μg/kg TP+0.2 mg/kg Compound C). Except sham group, rats in other groups were treated with ligation of left anterior descending coronary artery to establish HF model. Cardiac function indicators of rats in each group were detected by echocardiography. HE and TUNEL staining methods were used to detect pathological changes in rat myocardial tissue and myocardial cell apoptosis, respectively.ELISA was used to detect levels of brain natriuretic peptide, cardiac troponin I, tumor necrosis factor -α, interleukin-6 in rat myocardial tissue, as well as serum levels of malondialdehyde and superoxide dismutase. Western blotting was used to detect the AMPK/mTOR signaling pathway and apoptosis-related protein expression levels in rat myocardial tissue. ResultsThe heart function of HF rats were decreased, the apoptosis rate of myocardial cells were increased, the arrangement of myocardial tissue cells was disordered, the gaps became wider, the ventricular wall became thinner, and a large number of inflammatory cell infiltration and oxidative stress reactions occurred. The AMPK/mTOR signaling pathway was inhibited. After high-dose TP intervention, the heart function of HF rats was improved. Myocardial cell apoptosis, inflammatory response, and oxidative stress were alleviated, and the AMPK/mTOR signaling pathway was activated. The AMPK inhibitor Compound C weakened the improvement of TP on myocardial injury in HF rats. ConclusionTP may play a cardioprotective role in alleviating injury by activating AMPK/mTOR signaling pathway. |
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