發(fā)布時間：2019-05-24 14:21

【摘要】：研究背景:MicroRNAs(miRNAs或miRs)是一類長度為22個核苷酸的非編碼RNA,目前已知參與心血管生物學的各個方面,如心肌肥厚、心肌纖維化、心肌收縮和血管新生等。芪藶強心(qiliqiangxin,QL)提取物作為中國傳統(tǒng)中藥復方制劑,其成分由黃芪、人參、附子等組成。目前研究表明,芪藶強心通過調節(jié)mi RNAs從而在改善心力衰竭中起一系列病理生理作用,如增強心肌收縮、改善心肌重構、抑制細胞凋亡、改善心肌炎癥、促進血管新生等。人類心力衰竭的心肌細胞miR-25表達水平明顯增高,Wahlquist等通過抑制miR-25誘導SERCA2a表達水平治療逆轉小鼠胸主動脈縮窄術(TAC)模型誘導的心力衰竭。然而,芪藶強心是否通過調節(jié)mi R-25來發(fā)揮改善心力衰竭的作用鮮有報道。目的:觀察芪藶強心(Qiliqiangxin,QL)提取物對缺氧條件下誘導的心肌細胞(cadiomyocyte,CM)損傷的影響,探討芪藶強心提取物改善心肌損傷的相關機制。方法:原代培養(yǎng)乳鼠心肌細胞,進行缺氧及藥物干預處理。采用RT-PCR及Western Blot檢測mi R-25及其下游SERCA2a基因和SERCA2a蛋白表達水平,采用fluo 3-AM檢測細胞鈣離子濃度等結果:與對照組相比,缺氧組miR-25表達水平升高,SERCA2a基因及蛋白表達水平下降;與缺氧組比較,芪藶強心組miR-25下降,SERCA2a基因及蛋白表達水平升高。與缺氧組比較,芪藶強心組細胞內胞漿鈣離子濃度水平減少。結論:缺氧條件下,芪藶強心通過下調miR-25表達水平,上調SERCA2a基因和蛋白的表達,減少心肌細胞鈣離子濃度,改善細胞鈣超載,進而改善心肌細胞功能。
[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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