七氟醚后处理调控microRNA-133a表达对小鼠心肌缺血再灌注损伤的影响

发布时间：2018-08-08 13:39

【摘要】：目的:以七氟醚后处理为干预措施,探讨mi RNA-133a及凋亡相关蛋白在七氟醚心肌保护中的作用。方法:30只C57小鼠随机分为3组,即对照组(control,TC)、缺血/再灌注组(Ischemia/reperfusion,I/R)、七氟醚后处理组(Sevo+IR)。对照组只进行开胸,不结扎冠状动脉后关胸;缺血/再灌注组结扎冠状动脉成功后关胸,30min后松开结扎线,复灌180min。七氟醚后处理组结扎冠状动脉成功后关胸,30min后松开结扎线,并持续吸入2.4%七氟醚5min,复灌180min。心肌梗死的程度由乳酸脱氢酶(LDH)和肌酸激酶(CK)的水平以及心肌梗死面积说明;Western blot法检测Caspase-9的表达;RT-PCR法分别检测mi RNA-133a、Bax、Bcl-2及Caspase-9水平的变化。结果:七氟醚后处理能够减少缺血/再灌注损伤导致的左心室心梗面积,减少LDH及CK的水平。与缺血/再灌注组对比,七氟醚后处理组中心肌细胞凋亡显著减少(P0.05)。通过RT-PCR法测得心肌特异性Mi RNA-133a在缺血/再灌注时水平显著下降,经七氟醚后处理水平上升(P0.05);同时,七氟醚后处理下调凋亡相关蛋白Bax及Caspase-9的m RNA表达,上调Bcl-2的m RNA表达(P0.05)。Western blot也证实与缺血/再灌注组相比,七氟醚后处理组使Caspase-9的蛋白表达显著下降(P0.05)。结论:七氟醚后处理能够上调Micro RNA-133a的表达,减少细胞凋亡。Micro RNA-133a的抗细胞凋亡的靶点可能为Caspase-9。Micro RNA-133a参与七氟醚后处理的心肌保护作用,在其过程中扮演了重要的角色。
[Abstract]:Aim: to investigate the role of mi RNA-133a and apoptosis-related protein in the myocardial protection of sevoflurane by sevoflurane post-treatment. Methods Thirty C57 mice were randomly divided into three groups: control group, ischemia / reperfusion group and sevoflurane post-treatment group (Sevo IR). The patients in the control group only underwent thoracotomy without ligation of the coronary artery and the ischemia / reperfusion group loosened the ligation line 30 minutes after the successful ligation of the coronary artery and reperfused the coronary artery for 180 minutes. In the sevoflurane post-treatment group, the coronary artery was successfully ligated, the thoracic ligation was closed for 30 minutes, the ligation line was released, and 2.4% sevoflurane was inhaled continuously for 5 min, then reperfused for 180 min. The degree of myocardial infarction was determined by the levels of lactate dehydrogenase (LDH) and creatine kinase (CK) (CK) and the area of myocardial infarction (AMI). The expression of Caspase-9 was detected by Western blot. The expression of Caspase-9 was detected by RT-PCR. Results: after sevoflurane treatment, the area of left ventricular myocardial infarction and the levels of LDH and CK were reduced after ischemia / reperfusion injury. Compared with ischemia / reperfusion group, cardiac myocyte apoptosis was significantly decreased in sevoflurane post treatment group (P0.05). Myocardial specific Mi RNA-133a decreased significantly during ischemia / reperfusion and increased after sevoflurane treatment (P0.05), and the m RNA expression of apoptosis-related protein Bax and Caspase-9 was down-regulated by sevoflurane post-treatment. Upregulation of m RNA expression of Bcl-2 (P0.05). Western blot also confirmed that sevoflurane post-treated group significantly decreased the expression of Caspase-9 protein compared with ischemia / reperfusion group (P0.05). Conclusion: sevoflurane post treatment can up-regulate the expression of Micro RNA-133a and reduce the anti-apoptosis target of apoptosis. Micro RNA-133a may play an important role in the myocardial protection of sevoflurane.
【学位授予单位】：新疆医科大学
【学位级别】：硕士
【学位授予年份】：2016
【分类号】：R614

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