【摘要】：Myocardin可以誘導心肌肥厚,而一氧化氮(NO)對于心肌具有一定保護作用,但在心肌肥厚發(fā)生的過程中,NO的作用尚未報道.本文首先用NO熒光探針檢測亞硝基谷胱甘肽(S-Nitrosoglutathione,GSNO)處理能夠引起H9c2細胞中NO總含量的上升.隨后利用200,μmol/L GSNO處理細胞,檢測發(fā)現(xiàn)Myocardin可以發(fā)生亞硝�；揎�,同時心肌肥厚標志基因α-MHC在mRNA水平和蛋白水平的表達均下調(diào).最后通過熒光素酶報告分析、RT-PCR以及Western blot分析表明,過表達Myocardin可以激活GSNO還原酶(GSNO reductase,GSNOR)的表達,并且降低細胞內(nèi)NO總量.以上結(jié)果表明,亞硝�；梢砸种朴蒑yocardin誘導的心肌肥厚的發(fā)生,同時Myocardin可以激活GSNOR的轉(zhuǎn)錄,間接抑制GSNO對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實驗室天津市工業(yè)微生物重點實驗室天津科技大學生物工程學院;
【基金】：國家自然科學基金資助項目(31171303)
【分類號】：R542.2
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本文編號：2209777