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替米沙坦通过 miR-1 依赖途径对缺血/缺氧损伤起心脏保护作用。

Telmisartan cardioprotects from the ischaemic/hypoxic damage through a miR-1-dependent pathway.

机构信息

Department of Experimental Medicine, University of Campania 'Luigi Vanvitelli', Naples, Italy.

Department of Mental and Physical Health and Preventive Medicine, University of Campania 'Luigi Vanvitelli', Naples, Italy.

出版信息

J Cell Mol Med. 2019 Oct;23(10):6635-6645. doi: 10.1111/jcmm.14534. Epub 2019 Aug 1.

Abstract

The aim of this study was to investigate whether telmisartan protects the heart from the ischaemia/reperfusion damage through a local microRNA-1 modulation. Studies on the myocardial ischaemia/reperfusion injury in vivo and on the cardiomyocyte hypoxia/reoxygenation damage in vitro were done. In vivo, male Sprague-Dawley rats administered for 3 weeks with telmisartan 12 mg/kg/d by gastric gavage underwent ischaemia/reperfusion of the left descending coronary artery. In these rats, infarct size measurement, ELISA, immunohistochemistry (IHC) and reverse transcriptase real-time polymerase chain reaction showed that expressions of connexin 43, potassium voltage-gated channel subfamily Q member 1 and the protein Bcl-2 were significantly increased by telmisartan in the reperfused myocardium, paralleled by microRNA-1 down-regulation. In vitro, the transfection of cardiomyocytes with microRNA-1 reduced the expressions of connexin 43, potassium voltage-gated channel subfamily Q member 1 and Bcl-2 in the cells. Telmisartan (50 µmol/L) 60 minutes before hypoxia/reoxygenation, while not affecting the levels of miR-1 in transfected cells in normoxic condition, almost abolished the increment of miR-1 induced by the hypoxia/reoxygenation to transfected cells. All together, telmisartan cardioprotected against the myocardial damage through the microRNA-1 modulation, and consequent modifications of its downstream target connexin 43, potassium voltage-gated channel subfamily Q member 1 and Bcl-2.

摘要

本研究旨在探讨替米沙坦是否通过局部 microRNA-1 调节来保护心脏免受缺血/再灌注损伤。进行了体内心肌缺血/再灌注损伤和体外心肌细胞缺氧/复氧损伤研究。在体内,给予替米沙坦 12mg/kg/d 灌胃 3 周的雄性 Sprague-Dawley 大鼠进行左冠状动脉前降支缺血/再灌注。在这些大鼠中,通过梗死面积测量、ELISA、免疫组织化学(IHC)和逆转录实时聚合酶链反应显示,替米沙坦在再灌注心肌中显著增加了连接蛋白 43、钾电压门控通道亚家族 Q 成员 1 和蛋白 Bcl-2 的表达,同时下调了 microRNA-1 的表达。在体外,microRNA-1 转染降低了细胞中连接蛋白 43、钾电压门控通道亚家族 Q 成员 1 和 Bcl-2 的表达。替米沙坦在缺氧/复氧前 60 分钟(50µmol/L)给药,在正常氧条件下不影响转染细胞中 miR-1 的水平,但几乎完全消除了缺氧/复氧对转染细胞中 miR-1 诱导的增加。总之,替米沙坦通过 microRNA-1 调节,继而对其下游靶标连接蛋白 43、钾电压门控通道亚家族 Q 成员 1 和 Bcl-2 进行修饰,对心肌损伤起到保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be00/6787508/74a9cd150b90/JCMM-23-6635-g001.jpg

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