辛伐他汀对大鼠肾缺血再灌注损伤后心肌Bcl-2和Bax蛋白表达的影响
发布时间:2018-11-07 13:03
【摘要】:目的:观察辛伐他汀对肾缺血再灌注损伤后心肌组织的影响及其机制。方法:随机将36只大鼠分为假手术组、肾缺血再灌注组和辛伐他汀组,每组12只。后2组用夹闭双侧肾动脉的方法复制肾缺血再灌注损伤模型;辛伐他汀组在造模前给予辛伐他汀(20 mg·kg~(-1)·d~(-1))灌胃,持续2周。用生化检查检测血清肌酐(SCr)、血尿素氮(BUN)、心肌组织丙二醛(MDA)含量及乳酸脱氢酶(LDH)、肌酸激酶(CK)和超氧化物歧化酶(SOD)的活性,并用Western blot法检测Bcl-2和Bax的表达水平。结果:与假手术组比,缺血再灌注组SCr、BUN和心肌MDA含量均升高(P0.05),心肌LDH和CK活性增强(P0.05),心肌SOD活性明显下降(P0.05);与缺血再灌注组比较,辛伐他汀组SCr、BUN和心肌MDA的含量降低(P0.05),心肌LDH和CK活性明显减弱(P0.05),而心肌SOD活性增强(P0.05)。与假手术组比较,心肌Bcl-2与Bax的蛋白表达水平在肾缺血再灌注组增多(P0.05);与缺血组相比,Bax表达在辛伐他汀组明显降低,而Bcl-2表达增加(P0.05)。结论:辛伐他汀对肾缺血再灌注后的心肌有保护作用,保护机制可能与辛伐他汀可以消除自由基、升高Bcl-2蛋白表达和降低Bax蛋白表达有一定关系。
[Abstract]:Aim: to observe the effect and mechanism of simvastatin on myocardial tissue after renal ischemia reperfusion injury. Methods: Thirty-six rats were randomly divided into sham-operation group, renal ischemia reperfusion group and simvastatin group with 12 rats in each group. The model of renal ischemia-reperfusion injury was induced by clamping bilateral renal arteries in the latter two groups, and simvastatin (20 mg kg~ (-1) D1) was administered intragastrically for 2 weeks in simvastatin group. The contents of malondialdehyde (MDA) in serum creatinine (SCr),) and blood urea nitrogen (BUN), and the activities of lactate dehydrogenase (LDH), (LDH), creatine kinase (CK) and superoxide dismutase (SOD) were measured by biochemical examination. The expression levels of Bcl-2 and Bax were detected by Western blot method. Results: compared with sham-operation group, the contents of SCr,BUN and myocardial MDA in ischemia-reperfusion group were increased (P0.05), the activities of myocardial LDH and CK were increased (P0.05), and the activity of myocardial SOD was significantly decreased (P0.05). Compared with ischemia reperfusion group, simvastatin group decreased the content of SCr,BUN and myocardial MDA (P0.05), decreased myocardial LDH and CK activity (P0.05), and increased myocardial SOD activity (P0.05). Compared with sham operation group, the expression of Bcl-2 and Bax in myocardium increased in renal ischemia-reperfusion group (P0.05); compared with ischemic group, the expression of Bax decreased significantly in simvastatin group, while Bcl-2 expression increased (P0.05). Conclusion: simvastatin has protective effect on myocardium after renal ischemia-reperfusion, and the protective mechanism may be related to the action of simvastatin on eliminating free radicals, increasing the expression of Bcl-2 protein and decreasing the expression of Bax protein.
【作者单位】: 石家庄医学高等专科学校;
【基金】:河北省教育厅高等学校科学技术指导性研究项目(No.Z2014020)
【分类号】:R965
本文编号:2316453
[Abstract]:Aim: to observe the effect and mechanism of simvastatin on myocardial tissue after renal ischemia reperfusion injury. Methods: Thirty-six rats were randomly divided into sham-operation group, renal ischemia reperfusion group and simvastatin group with 12 rats in each group. The model of renal ischemia-reperfusion injury was induced by clamping bilateral renal arteries in the latter two groups, and simvastatin (20 mg kg~ (-1) D1) was administered intragastrically for 2 weeks in simvastatin group. The contents of malondialdehyde (MDA) in serum creatinine (SCr),) and blood urea nitrogen (BUN), and the activities of lactate dehydrogenase (LDH), (LDH), creatine kinase (CK) and superoxide dismutase (SOD) were measured by biochemical examination. The expression levels of Bcl-2 and Bax were detected by Western blot method. Results: compared with sham-operation group, the contents of SCr,BUN and myocardial MDA in ischemia-reperfusion group were increased (P0.05), the activities of myocardial LDH and CK were increased (P0.05), and the activity of myocardial SOD was significantly decreased (P0.05). Compared with ischemia reperfusion group, simvastatin group decreased the content of SCr,BUN and myocardial MDA (P0.05), decreased myocardial LDH and CK activity (P0.05), and increased myocardial SOD activity (P0.05). Compared with sham operation group, the expression of Bcl-2 and Bax in myocardium increased in renal ischemia-reperfusion group (P0.05); compared with ischemic group, the expression of Bax decreased significantly in simvastatin group, while Bcl-2 expression increased (P0.05). Conclusion: simvastatin has protective effect on myocardium after renal ischemia-reperfusion, and the protective mechanism may be related to the action of simvastatin on eliminating free radicals, increasing the expression of Bcl-2 protein and decreasing the expression of Bax protein.
【作者单位】: 石家庄医学高等专科学校;
【基金】:河北省教育厅高等学校科学技术指导性研究项目(No.Z2014020)
【分类号】:R965
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,本文编号:2316453
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