| 强心汤通过BNIP3/NIX/FUNDC1途径介导心肌线粒体自噬对慢性心力衰竭大鼠心肌纤维化的影响 |
| 投稿时间：2024-08-14 修订日期：2024-08-28 点此下载全文 |
| 引用本文：庞延,陈佳永,毛美玲,董礼,张因彪.强心汤通过BNIP3/NIX/FUNDC1途径介导心肌线粒体自噬对慢性心力衰竭大鼠心肌纤维化的影响[J].医学研究杂志,2025,54(1):43-47 |
| DOI：
10.11969/j.issn.1673-548X.2025.01.009 |
| 摘要点击次数: 136 |
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| 基金项目:广西自然科学基金资助项目(2021GXNSFBA196018);国家自然科学基金地区基金资助项目(82160887)；国家中医临床研究基地业务建设第二批科研专项(JDZX2015146)；国家中医药传承创新中心项目(2023019-10)；广西中医药管理局自筹经费科研课题(GXZYA20230065);广西高水平中医药重点学科-中医心病学(2024016-02-02)；广西岐黄学者培养项目(2022015-003-02) |
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| 中文摘要:目的 探讨强心汤通过Bcl-2/腺病毒E1B19kD相互作用蛋白3(BCL2/adenovirus E1B 19kDa interacting protein 3,BNIP3)/Nip3样蛋白X(NIP3-like protein X,NIX)、含FUN14结构域蛋白1(FUN14domain containing protein 1,FUNDC1)途径介导心肌线粒体自噬对慢性心力衰竭(chronic heart failure,CHF)大鼠心肌纤维化的影响。方法 40只SD(Sprague Dawley)大鼠按随机数字表法随机分为假手术组、模型组、强心汤组、卡托普利组、强心汤+卡托普利组共5组,每组8只,除假手术组只穿线不结扎心脏左冠状动脉以外,余各组均通过结扎心脏左冠状动脉建立心肌梗死后CHF大鼠模型,于造模成功后次日开始,各组分别给予相应的药物灌胃后,对各组大鼠左心室心肌组织进行检测,Western blot法检测各组NIX、BNIP3、FUNDC1蛋白表达,ELISA检测脑钠肽(brain natriuretic peptide,BNP)、心肌肌钙蛋白T(cardiac troponin T,cTnT)水平,透射电镜观察线粒体形态,Masson染色观察左心室心肌纤维化情况。结果 与假手术组比较,模型组NIX、BNIP3、FUNDC1蛋白表达明显降低,BNP、cTnT含量水平明显升高(P＜0.05),左心室心肌组织明显纤维化,线粒体肿胀；与模型组比较,强心汤组和卡托普利组NIX、BNIP3、FUNDC1蛋白表达明显升高,BNP、cTnT含量水平明显下降(P＜0.05),左心室心肌组织纤维化明显减轻,线粒体形态轻度改变,与强心汤组和卡托普利组比较,强心汤+卡托普利组上述指标明显改善,强心汤组与卡托普利组各指标比较,差异无统计学意义。结论 强心汤可能通过上调NIX、BNIP3、FUNDC1表达促进线粒体自噬保证线粒体形态功能,发挥减少心肌损伤和纤维化的作用,此外,强心汤联合卡托普利治疗CHF获益更佳。 |
| 中文关键词:慢性心力衰竭 强心汤 线粒体自噬 BNIP3/NIX/FUNDC1 心肌纤维化 |
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| Impact of Qiangxin Tang on Myocardial Fibrosis in Rats with Chronic Heart Failure Mediated by BNIP3/NIX/FUNDC1Pathway and Myocardial Mitochondrial Autophagy. |
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| Abstract:Objective To explore the impact of Qiangxin Tang on myocardial fibrosis in rats with chronic heart failure by mediating myocardial mitochondrial autophagy through the Bcl-2/adenovirus E1B 19kDa interacting protein 3/NIP3 like protein X and FUN14domain-containing protein 1. Methods Forty Sprague Dawley rats were divided into five groups randomly by the random number table:sham operation group, model group, Qiangxin Tang group, Captopril group, and Qiangxin Tang+Captopril group, with a total of eight rats in each group. Only the sham operation group threaded without ligating the left coronary artery of the heart. In all the other groups, CHF rat models were established after myocardial infarction by ligating the left coronary artery of the heart. From the day after successful modeling, each group was given corresponding drugs by gavage, and the left ventricular myocardial tissue of each group was detected. Western blot was used to detect the expression of NIX, BNIP3, and FUNDC1 proteins in each group. ELISA was used to detect brain natriuretic peptide and cardiac troponin T level. Mitochondrial morphology was observed under transmission electron microscopy. Masson staining was used to observe left ventricular myocardial fibrosis. Results Compared with the sham surgery group, the expression of NIX, BNIP3 and FUNDC1 proteins in the model group was significantly reduced, while the levels of BNP and cTnT were significantly increased (P<0.05). The left ventricular myocardial tissue showed significant fibrosisand mitochondrial swelling. Compared with the model group, the expression of NIX, BNIP3, and FUNDC1 proteins was significantly increased in Qiangxin Tang group and Captopril group, while the levels of BNP and cTnT were significantly decreased (P<0.05). The left ventricular myocardial tissue fibrosis was significantly reduced, and the mitochondrial morphology was mildly altered. Compared with Qiangxin Tang group and Captopril group, the Qiangxin Tang+Captopril group showed significant improvement in the above indicators, and there was no significant difference in the indicators between Qiangxin Tang group and Captopril group. Conclusion Qiangxin Tang may promote mitochondrial autophagy and ensure the morphology and function of mitochondrial by upregulating the expression of NIX, BNIP3 and FUNDC1, thereby reducing myocardial injury and fibrosis. In addition, the combination of Qiangxin Tang and Captopril has a better therapeutic effect on CHF. |
| keywords:Chronic heart failure Qiangxin Tang Mitochondrial autophagy BNIP3/NIX/FUNDC1 Myocardial fibrosis |
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