首页> 中文期刊>中国病理生理杂志 >辛伐他汀对大鼠肾缺血再灌注损伤后心肌rBcl-2和Bax蛋白表达的影响

辛伐他汀对大鼠肾缺血再灌注损伤后心肌rBcl-2和Bax蛋白表达的影响

     

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(P<0.05),心肌LDH和CK活性增强(P<0.05),心肌SOD活性明显下降(P<0.05);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(P<0.05),心肌LDH和CK活性明显减弱(P<0.05),而心肌SOD活性增强(P<0.05).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(P<0.05);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(P<0.05).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.%AIM:To observe the effect of simvastatin on myocardial tissue after renal ischemia-reperfusion in-jury and its mechanism .METHODS:A rat model of renal ischemia-reperfusion injury was prepared by clamping the bilat-eral renal arteries for 45 min.The rats (n=36) were randomly divided into sham operation group , renal ischemia-reperfu-sion (I/R) group and simvastatin group with 12 rats in each group.The content of serum creatinine (SCr), blood urea ni-trogen ( BUN) and myocardial tissue malondialdehyde ( MDA) , the myocardial activity of lactate dehydrogenase ( LDH) , creatine kinase (CK) and superoxide dismutase (SOD), and the myocardial protein expression of Bcl-2 and Bax were de-tected.RESULTS:Compared with sham operation group , the content of SCr , BUN and myocardial MDA , and the myo-cardial activity of LDH and CK in I/R group were significantly increased (P<0.05), and the activity of SOD was signifi-cantly decreased (P<0.05).Compared with I/R group, the content of SCr, BUN and myocardial MDA, and the myocar-dial activity of LDH and CK in simvastatin group were significantly decreased ( P<0.05 ) , while SOD activity was en-hanced (P<0.05).The protein expression of Bcl-2 and Bax in sham operation group was less than that in I/R group (P<0.05), and the protein level of Bax in simvastatin group was significantly lower than that in I /R group (P<0.05), while the protein level of Bcl-2 was increased (P<0.05).CONCLUSION:Simvastatin has a protective effect on the my-ocardium of the rats with renal ischemia-reperfusion injury , and the protective mechanism may be related to the elimination of free radicals by simvastatin , increase in the protein expression of Bcl-2 and decrease in the protein expression of Bax .

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