本文選題：組蛋白去乙�；� + 心臟擴(kuò)大��； 參考：《中國循環(huán)雜志》2017年08期

【摘要】：目的:探討組蛋白去乙�；�(HDAC)抑制劑辛二酰苯胺異羥肟酸(SAHA)改善小鼠心肌肥厚的作用,為防治心肌肥厚提供新思路。方法:選取60只昆明小鼠,隨機(jī)分為正常組、假手術(shù)組、心肌肥厚組、心肌肥厚+SAHA組,通過部分結(jié)扎小鼠胸主動脈建立心肌肥厚模型,最終每組納入6只。采用蘇木素伊紅(HE)染色觀察小鼠心肌細(xì)胞,超聲心動圖檢測小鼠心功能,比色法檢測HDAC活性,小鼠心肌組織中HDAC亞型HDAC5和β-肌球蛋白重鏈(β-MHC)信使核糖核酸(mRNA)和蛋白表達(dá)水平分別運(yùn)用逆轉(zhuǎn)錄-聚合酶鏈反應(yīng)(RT-PCR)和蛋白免疫印跡(Western blot)檢測。結(jié)果:HE染色結(jié)果表明心肌肥厚組小鼠心肌細(xì)胞肥大、排列紊亂、細(xì)胞核深染。心肌肥厚組小鼠左心室舒張末期直徑、左心室舒張末期容積均顯著低于假手術(shù)組(P0.05),而室間隔明顯較假手術(shù)組增厚(P0.05)。心肌肥厚組小鼠HDACs活性顯著高于假手術(shù)組(P0.05);心肌肥厚組HDAC5和β-MHC的mRNA及蛋白表達(dá)水平均顯著高于假手術(shù)組(P0.05)。SAHA能夠顯著降低HDAC5表達(dá)水平,顯著下調(diào)心臟肥厚相關(guān)基因β-MHC的表達(dá)并改善小鼠心功能和心肌肥厚(P均0.05)。結(jié)論:HDAC參與了心肌肥厚的發(fā)生,HDAC抑制劑SAHA通過抑制HDAC5的表達(dá)從而改善小鼠心肌肥厚。
[Abstract]:Aim: to investigate the effect of histone deacetylase (HDAC) inhibitor, octylaniline hydroxamic acid (SAHAA), on myocardial hypertrophy in mice, and to provide a new idea for prevention and treatment of myocardial hypertrophy. Methods: sixty Kunming mice were randomly divided into normal group, sham operation group, myocardial hypertrophy group and myocardial hypertrophy SAHA group. Myocardial hypertrophy model was established by partial ligation of thoracic aorta of mice. The cardiac myocytes of mice were observed by hematoxylin eosin (HEH) staining, the cardiac function of mice was detected by echocardiography, and the activity of HDAC was detected by colorimetric method. The expression of HDAC subtype HDAC5 and 尾 -myosin heavy chain (尾 -MHCM) mRNA mRNA and protein were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting (Western blot), respectively. Results the results showed that the cardiac myocytes in the hypertrophic group were hypertrophic, disordered, and the nuclei were deeply stained. The left ventricular end-diastolic diameter and left ventricular end-diastolic volume in the hypertrophic group were significantly lower than those in the sham operation group (P 0.05), while the ventricular septum was significantly thicker than that in the sham operation group. The expression of mRNA and protein in HDAC5 and 尾 -MHC in myocardial hypertrophy group was significantly higher than that in sham operation group, and the expression level of mRNA and protein in HDAC5 and 尾 -MHC in myocardial hypertrophy group was significantly higher than that in sham operation group. The expression of cardiac hypertrophy related gene 尾 -MHC was significantly down-regulated and the cardiac function and cardiac hypertrophy were significantly improved in mice. Conclusion SAHA is involved in the pathogenesis of myocardial hypertrophy and can improve myocardial hypertrophy by inhibiting the expression of HDAC5 in mice.
【作者單位】： 遵義醫(yī)學(xué)院附屬醫(yī)院兒內(nèi)科;遵義醫(yī)學(xué)院生理教研室;
【基金】：國家自然科學(xué)基金項(xiàng)目(81560040) 遵義醫(yī)學(xué)院博士啟動基金項(xiàng)目[院字(2015)4號] 遵義醫(yī)學(xué)院與科技學(xué)院大學(xué)生創(chuàng)新訓(xùn)練項(xiàng)目[遵醫(yī)科院(2015)3108]
【分類號】：R542.2

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