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目的:探讨组蛋白乙酰化修饰失衡在2种不同方法建立小鼠心肌肥厚模型中的作用。方法:选取昆明小鼠为研究对象,按照随机数字表法随机分为5组:正常组、0.9%氯化钠溶液组、苯肾上腺素组、手术组和假手术组。苯肾上腺素组给予苯肾上腺素皮下注射,手术组给予部分结扎腹主动脉建立小鼠心肌肥厚模型,实时荧光定量聚合酶链反应(real-time polymerase chain reaction,RT-PCR)检测心肌肥厚相关标志物心房利钠肽(atrial natriuretic peptide,ANP)及β-肌球蛋白重链(β-myosin heavy chain,β-MHC)mRNA表达水平,免疫印迹(western blot,WB)检测小鼠心肌组织中组蛋白H3赖氨酸残基9位乙酰化(H3K9ac)的表达,比色法检测心肌组织中组蛋白乙酰化酶(histone acetylases,HATs)、组蛋白去乙酰化酶(histone deacetylases,HDACs)活性,超声心动图观察小鼠心肌肥厚情况。结果:RT-PCR结果表明苯肾上腺素组、手术组小鼠心肌组织中ANP和β-MHC mRNA表达水平分别显著高于0.9%氯化钠溶液组、假手术组(P<0.05);超声心动图结果显示苯肾上腺素组、手术组小鼠室间隔厚度、左室前壁厚度分别显著高于0.9%氯化钠溶液组、假手术组(P<0.05),而左室舒张末期直径则分别显著低于0.9%氯化钠溶液组、假手术组(P<0.05)。Western blot及比色法结果显示:苯肾上腺素组、手术组小鼠心肌组织中组蛋白H3K9ac的乙酰化水平及HATs活性分别显著高于0.9%氯化钠溶液组、假手术组(P<0.05),而HDACs活性则分别显著低于0.9%氯化钠溶液组、假手术组(P<0.05)。结论:组蛋白乙酰化修饰失衡均参与了2种不同方式所致的小鼠心肌肥厚。
AIM: To investigate the role of histone acetylation imbalance in the establishment of mouse model of cardiac hypertrophy by two different methods. Methods: Kunming mice were selected as research objects and randomly divided into five groups according to random number table: normal group, 0.9% sodium chloride solution group, phenylephrine group, operation group and sham operation group. Phenylephrine was injected subcutaneously into the phenylephrine group. The rats in the operation group were given partial ligation of the abdominal aorta to establish a model of cardiac hypertrophy in mice. Real-time quantitative polymerase chain reaction (RT-PCR) The expressions of atrial natriuretic peptide (ANP) and β-myosin heavy chain (β-MHC) mRNA in the myocardium were detected by Western blot (WB) The protein H3 H3K9ac was detected by colorimetric assay. The activity of histone acetylases (HATs), histone deacetylases (HDACs) Echocardiography observed cardiac hypertrophy in mice. Results: RT-PCR results showed that the expression levels of ANP and β-MHC mRNA in the phenylephrine group and the operation group were significantly higher than those in 0.9% sodium chloride solution group and sham operation group (P <0.05) The results showed that the interventricular septum thickness and left anterior wall thickness in the phenylephrine group and the surgery group were significantly higher than those in the 0.9% sodium chloride solution group and the sham operation group (P <0.05), while the diameters of the left ventricular end diastole Significantly lower than 0.9% sodium chloride solution group, sham operation group (P <0.05). The results of Western blot and colorimetric assay showed that the histone H3K9ac acetylation level and HATs activity in the myocardium of the phenylephrine group and the operation group were significantly higher than those of the 0.9% sodium chloride solution group and the sham operation group (P <0.05) ), While the activities of HDACs were significantly lower than 0.9% sodium chloride solution group, sham operation group (P <0.05). CONCLUSION: Unbalanced histone acetylation is involved in cardiac hypertrophy in two different ways.