【摘要】：研究背景:MicroRNAs(miRNAs或miRs)是一類(lèi)長(zhǎng)度為22個(gè)核苷酸的非編碼RNA,目前已知參與心血管生物學(xué)的各個(gè)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(qiáng)心(qiliqiangxin,QL)提取物作為中國(guó)傳統(tǒng)中藥復(fù)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(qiáng)心通過(guò)調(diào)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(qiáng)心肌收縮、改善心肌重構(gòu)、抑制細(xì)胞凋亡、改善心肌炎癥、促進(jìn)血管新生等。人類(lèi)心力衰竭的心肌細(xì)胞miR-25表達(dá)水平明顯增高,Wahlquist等通過(guò)抑制miR-25誘導(dǎo)SERCA2a表達(dá)水平治療逆轉(zhuǎn)小鼠胸主動(dòng)脈縮窄術(shù)(TAC)模型誘導(dǎo)的心力衰竭。然而,芪藶強(qiáng)心是否通過(guò)調(diào)節(jié)mi R-25來(lái)發(fā)揮改善心力衰竭的作用鮮有報(bào)道。目的:觀察芪藶強(qiáng)心(Qiliqiangxin,QL)提取物對(duì)缺氧條件下誘導(dǎo)的心肌細(xì)胞(cadiomyocyte,CM)損傷的影響,探討芪藶強(qiáng)心提取物改善心肌損傷的相關(guān)機(jī)制。方法:原代培養(yǎng)乳鼠心肌細(xì)胞,進(jìn)行缺氧及藥物干預(yù)處理。采用RT-PCR及Western Blot檢測(cè)mi R-25及其下游SERCA2a基因和SERCA2a蛋白表達(dá)水平,采用fluo 3-AM檢測(cè)細(xì)胞鈣離子濃度等結(jié)果:與對(duì)照組相比,缺氧組miR-25表達(dá)水平升高,SERCA2a基因及蛋白表達(dá)水平下降;與缺氧組比較,芪藶強(qiáng)心組miR-25下降,SERCA2a基因及蛋白表達(dá)水平升高。與缺氧組比較,芪藶強(qiáng)心組細(xì)胞內(nèi)胞漿鈣離子濃度水平減少。結(jié)論:缺氧條件下,芪藶強(qiáng)心通過(guò)下調(diào)miR-25表達(dá)水平,上調(diào)SERCA2a基因和蛋白的表達(dá),減少心肌細(xì)胞鈣離子濃度,改善細(xì)胞鈣超載,進(jìn)而改善心肌細(xì)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，

本文編號(hào)：2484935