芪苈强心提取物下调microRNA-25改善缺氧诱导的心肌细胞损伤

发布时间：2019-05-24 14:21

【摘要】：研究背景:MicroRNAs(miRNAs或miRs)是一类长度为22个核苷酸的非编码RNA,目前已知参与心血管生物学的各个方面,如心肌肥厚、心肌纤维化、心肌收缩和血管新生等。芪苈强心(qiliqiangxin,QL)提取物作为中国传统中药复方制剂,其成分由黄芪、人参、附子等组成。目前研究表明,芪苈强心通过调节mi RNAs从而在改善心力衰竭中起一系列病理生理作用,如增强心肌收缩、改善心肌重构、抑制细胞凋亡、改善心肌炎症、促进血管新生等。人类心力衰竭的心肌细胞miR-25表达水平明显增高,Wahlquist等通过抑制miR-25诱导SERCA2a表达水平治疗逆转小鼠胸主动脉缩窄术(TAC)模型诱导的心力衰竭。然而,芪苈强心是否通过调节mi R-25来发挥改善心力衰竭的作用鲜有报道。目的:观察芪苈强心(Qiliqiangxin,QL)提取物对缺氧条件下诱导的心肌细胞(cadiomyocyte,CM)损伤的影响,探讨芪苈强心提取物改善心肌损伤的相关机制。方法:原代培养乳鼠心肌细胞,进行缺氧及药物干预处理。采用RT-PCR及Western Blot检测mi R-25及其下游SERCA2a基因和SERCA2a蛋白表达水平,采用fluo 3-AM检测细胞钙离子浓度等结果:与对照组相比,缺氧组miR-25表达水平升高,SERCA2a基因及蛋白表达水平下降;与缺氧组比较,芪苈强心组miR-25下降,SERCA2a基因及蛋白表达水平升高。与缺氧组比较,芪苈强心组细胞内胞浆钙离子浓度水平减少。结论:缺氧条件下,芪苈强心通过下调miR-25表达水平,上调SERCA2a基因和蛋白的表达,减少心肌细胞钙离子浓度,改善细胞钙超载,进而改善心肌细胞功能。
[Abstract]:Background: MicroRNAs (miRNAs or miRs) is a class of non-coding RNA, with a length of 22 nucleotides, which is known to be involved in various aspects of cardiovascular biology, such as myocardial hypertrophy, myocardial fibrosis, myocardial contraction and neovascularization. Qiliqiangxin (qiliqiangxin,QL) extract, as a traditional Chinese medicine compound preparation, is composed of Astragalus membranaceus, ginseng, aconite and so on. Current studies have shown that Qiliqiangxin plays a series of pathophysiological roles in improving heart failure by regulating mi RNAs, such as enhancing myocardial contraction, improving myocardial remodeling, inhibiting apoptosis, improving myocardial inflammation, promoting neovascularization and so on. The expression of miR-25 in cardiomyocytes of human heart failure was significantly increased. Wahlquist et al., by inhibiting the expression of SERCA2a induced by miR-25, reversed the heart failure induced by (TAC) model of thoracic aortic constriction in mice. However, it is rarely reported whether Qiliqiang plays an important role in improving heart failure by regulating mi R 鈮，

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