| 黄芪甲苷激活ROCK/JNK介导自噬减轻异丙肾上腺素诱导的小鼠心肌纤维化 |
| 投稿时间：2022-12-28 修订日期：2023-06-04 点此下载全文 |
| 引用本文：武菲菲,张绡绮,连敬,杨晶,翟蒙恩,乔锐,徐臣年,杨婷婷.黄芪甲苷激活ROCK/JNK介导自噬减轻异丙肾上腺素诱导的小鼠心肌纤维化[J].药学实践杂志,2023,41(8):478~484 |
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| 基金项目:国家自然科学基金青年项目（82100513）；辽宁省2023年第一批中央引导地方科技发展资金 （2023JH6/100100034）；沈阳市科学技术计划基金资助项目（20-205-4-039） |
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| 中文摘要:目的 探讨黄芪甲苷（AS-Ⅳ）激活ROCK/JNK调控自噬，改善异丙肾上腺素（ISO）诱导的小鼠心肌纤维化(MF)的作用及机制。方法 将小鼠随机分为对照组、ISO诱导心肌纤维化组（MF组）、黄芪甲苷组、黄芪甲苷与Y-33075（ROCK抑制剂）联合组（黄芪甲苷+Y-33075组），重复给药持续30 d后，检测小鼠血清LDH、BNP、CTGF水平，超声检测心功能指标，天狼猩红、Masson染色检测各组小鼠心肌结构及组织纤维化程度， DHE检测各组小鼠心肌组织氧化应激（ROS）水平，蛋白印迹法检测心肌组织ROCK、JNK、Atg5、Beclin 1、LC3 Ⅰ/Ⅱ表达。结果 与黄芪甲苷组比较，黄芪甲苷+Y-33075组的EF值降低，心肌纤维化程度增加，血清LDH、BNP、CTGF水平升高，心肌组织ROS水平增高，ROCK、JNK、Atg5、Beclin 1、LC3 Ⅰ/Ⅱ表达水平表达降低（P<0.05），表明Y-33075能够阻断黄芪甲苷对心肌纤维化的保护作用，并抑制黄芪甲苷对ROCK和JNK的调控。结论 黄芪甲苷通过激活ROCK/JNK信号促进自噬减轻小鼠心肌纤维化。 |
| 中文关键词:心肌纤维化 自噬 ROCK/JNK 黄芪甲苷 小鼠 |
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| Alleviation of isoproterenol-induced myocardial fibrosis in mice by autophagy regulated by Astragaloside Ⅳ through activating ROCK/JNK pathway |
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| Abstract:Objective To investigate the effect and mechanism of astragaloside Ⅳ(AS-Ⅳ) activating ROCK/JNK to regulate autophagy in improving isoproterenol (ISO) induced myocardial fibrosis (MF) in mice. Methods The mice were randomly divided into control operation group (Control group), ISO induced myocardial fibrosis group (MF group), AS-Ⅳ treatment group (AS-Ⅳ group) and combination group of astragaloside IV and Y-33075 (ROCK inhibitor) (astragaloside IV+Y-33075 group). After repeated administration for 30 days. The serum levels of LDH, BNP, CTGF in each group were detected. The cardiac function was detected by ultrasound. Myocardial structure and tissue fibrosis degree in each group were detected by Sirius Red and Masson staining. Oxidative stress (ROS) levels in myocardial tissue of each group were detected by DHE staining and the expression of ROCK, JNK, Atg5, Beclin 1, and LC3 Ⅰ/Ⅱ in myocardial tissue were detected by Western blotting. Results Compared with AS-Ⅳ group, the EF value of AS-Ⅳ+Y-33075 group decreased and the degree of myocardial fibrosis increased (P<0.05). The serum level of LDH, BNP, CTGF increased and the level of ROS in myocardial tissue increased while the expression of ROCK, JNK, Atg5, Beclin 1, LC3 Ⅰ/Ⅱ decreased (P<0.05). Y-33075 could block the protective effect of AS-Ⅳ on myocardial injury induced by MF and inhibit the regulation of AS-Ⅳ on ROCK and JNK. Conclusion AS-Ⅳ could attenuate myocardial fibrosis in mice by activating ROCK/JNK signal and promoting autophagy. |
| keywords:myocardial fibrosis autophagy ROCK/JNK astragaloside Ⅳ mice |
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