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HDAC3在H9C2细胞缺血再灌注损伤中的表达及干预机制 被引量:1

Role of HDAC3 in H9C2 cell ischemia-reperfusion injury and intervention mechanism
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摘要 目的探讨组蛋白去乙酰化酶3(HDAC3)在大鼠H9C2心肌细胞缺血再灌注损伤中的表达及其部分机制研究。方法将H9C2细胞分为以下3组:正常对照组、缺血/再灌注(I/R)组、I/R+曲古霉素(TSA)组。MTT法检测细胞增殖活力;检测培养液中乳酸脱氢酶(LDH)水平;Western blot法测定细胞内HDAC3蛋白表达水平;实时荧光定量PCR检测HDAC3 mRNA表达情况。结果 MTT法检测结果显示:与正常对照组比较,I/R组、I/R+TSA组抑制率均显著提高,并且I/R组显著高于I/R+TSA组;I/R组LDH活性明显高于正常对照组,I/R+TSA组显著低于I/R组;Western blot检测显示:I/R组、I/R+TSA组HDAC3的表达明显高于正常对照组,I/R+TSA组显著低于I/R组;实时荧光定量PCR检测I/R组、I/R+TSA组HDAC3的mRNA表达明显高于正常对照组,I/R+TSA组显著低于I/R组。结论HDAC3表达上调可能在H9C2细胞缺血再灌注损伤中起到重要作用。 Objective To investigate the expression and the role of histone deacetylase 3 ( HDAC3 ) on H9C2 cell ischemia reperfusion injury. Methods H9C2 myocardial cells were divided into 3 groups randomly : control group, I/R group, I/R + TSA group. The cell viability was detected by M3T. Lactate dehydrogenase(LDH) level was de- tected in culture. The protein expression of HDAC3 was tested by Western blot. The mRNA expression of HDAC3 was examined by qRT-PCR. Results MTF assay showed that cell viability decreased significantly in I/R group compared with the control group, increased significantly in I/R + TSA group compared with I/R group. The content of LDH in cell activity increased significantly in I/R group compared with the control group, decreased significantly in I/R + TSA group compared with I/R group. Western blot indicated that the protein expression of HDAC3 in I/R group was higher than the control group, the expression of HDAC3 in I/R + TSA group was lower than I/R group. qRT-PCR indicated that the mRNA expression of HDAC3 in I/R group was higher than the control group, the ex- pression of HDAC3 in I/R + TSA group was lower than that in I/R group. Conclusion Upregulated HDAC3 plays an important role in H9C2 cell ischemia reperfusion injury.
出处 《安徽医科大学学报》 CAS 北大核心 2017年第5期674-677,共4页 Acta Universitatis Medicinalis Anhui
基金 国家自然科学基金项目(编号:81570295) 安徽省科技攻关项目(编号:1501041148) 安徽省高校自然科学研究项目(编号:KJ2015A320)
关键词 缺血再灌注损伤 组蛋白去乙酰化酶3 H9C2细胞 ischemia reperfusion injury HDAC3 myocardial cell
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