【摘要】：Myocardin可以誘導(dǎo)心肌肥厚,而一氧化氮(NO)對(duì)于心肌具有一定保護(hù)作用,但在心肌肥厚發(fā)生的過(guò)程中,NO的作用尚未報(bào)道.本文首先用NO熒光探針檢測(cè)亞硝基谷胱甘肽(S-Nitrosoglutathione,GSNO)處理能夠引起H9c2細(xì)胞中NO總含量的上升.隨后利用200,μmol/L GSNO處理細(xì)胞,檢測(cè)發(fā)現(xiàn)Myocardin可以發(fā)生亞硝�；揎�,同時(shí)心肌肥厚標(biāo)志基因α-MHC在mRNA水平和蛋白水平的表達(dá)均下調(diào).最后通過(guò)熒光素酶報(bào)告分析、RT-PCR以及Western blot分析表明,過(guò)表達(dá)Myocardin可以激活GSNO還原酶(GSNO reductase,GSNOR)的表達(dá),并且降低細(xì)胞內(nèi)NO總量.以上結(jié)果表明,亞硝�；梢砸种朴蒑yocardin誘導(dǎo)的心肌肥厚的發(fā)生,同時(shí)Myocardin可以激活GSNOR的轉(zhuǎn)錄,間接抑制GSNO對(duì)Myocardin的作用.
[Abstract]:Myocardin can induce myocardial hypertrophy, but nitric oxide (NO) has a protective effect on myocardium, but the role of no in the process of myocardial hypertrophy has not been reported. In this paper, NO fluorescence probe was used to detect that S-Nitrosoglutathione glutathione (GSNO) treatment could increase the total NO content in H9c2 cells. After treated with 200 渭 mol/L GSNO, it was found that Myocardin could be modified by nitrite, and the expression of 偽 -MHC, a marker of myocardial hypertrophy, was down-regulated at the level of mRNA and protein. Finally, RT-PCR and Western blot analysis showed that overexpression of Myocardin could activate the expression of GSNO reductase (GSNO reductase,GSNOR) and decrease the total amount of NO in cells. These results suggest that nitrite can inhibit the occurrence of myocardial hypertrophy induced by Myocardin and that Myocardin can activate the transcription of GSNOR and indirectly inhibit the effect of GSNO on Myocardin.
【作者單位】： 工業(yè)發(fā)酵微生物教育部重點(diǎn)實(shí)驗(yàn)室天津市工業(yè)微生物重點(diǎn)實(shí)驗(yàn)室天津科技大學(xué)生物工程學(xué)院;
【基金】：國(guó)家自然科學(xué)基金資助項(xiàng)目(31171303)
【分類號(hào)】：R542.2
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本文編號(hào)：2209777