CAJ | 학술논문

目的探讨PEP-1超氧化物歧化酶(SOD1)融合蛋白对大鼠心肌缺血再灌注细胞凋亡指数、Bax和Bcl-2蛋白表达的影响.方法 SD大鼠40只,制作心肌缺血再灌注模型,分为假手术组、缺血再灌注组、PEP-1-SOD1 100、300和500 μg组,每组8只.TUNEL法及免疫组织化学法检测心肌细胞凋亡指数(AI)及Bax、Bcl-2蛋白的表达.结果假手术组AI、Bax及Bcl-2蛋白表达水平均较低.PEP-1-SOD1各组AI和Bax蛋白的表达较缺血再灌注组明显降低,Bcl-2蛋白的表达明显增加,Bax/Bcl-2比值明显下降(P<0.05,P<0.01).结论 PEP-1-SOD1可抑制缺血再灌注心肌细胞凋亡,原因可能为其减轻氧化应激、下调Bax和上调Bcl-2蛋白表达水平.
목적 탐토PEP-1초양화물기화매(SOD1)융합단백대대서심기결혈재관주세포조망지수、Bax화Bcl-2단백표체적영향.방법 SD대서40지,제작심기결혈재관주모형,분위가수술조、결혈재관주조、PEP-1-SOD1 100、300화500 μg조,매조8지.TUNEL법급면역조직화학법검측심기세포조망지수(AI)급Bax、Bcl-2단백적표체.결과 가수술조AI、Bax급Bcl-2단백표체수평균교저.PEP-1-SOD1각조AI화Bax단백적표체교결혈재관주조명현강저,Bcl-2단백적표체명현증가,Bax/Bcl-2비치명현하강(P<0.05,P<0.01).결론 PEP-1-SOD1가억제결혈재관주심기세포조망,원인가능위기감경양화응격、하조Bax화상조Bcl-2단백표체수평.
Objective To explore the influence of PEP-1-SOD1 fusion protein on cardiomyocyte ap-optosis, expression of Bax and Bcl-2 proteins following myocardial ischemia-reperfusion in rats.Methods Forty rats were randomly divided into sham-operated group, ischemia-reperfusion group,PEP-1-SOD1 100,300 and 500 μg groups(8 rats in each group). Ischemia-reperfusion mod-el was established by left anterior descending coronary artery ligation for 1 h,followed by 2 h of reperfusion. Cardiomyocyte apoptotic index(AI),Bax and Bcl-2 in cardiomyocytes were detected with TUNEL and immunohistochemistry methods, respectively. Results The levels of AI,Bax and Bcl-2 proteins were low in sham-operated group. In. PEP-1-SOD1 groups, the levels of AI,Bax and Bax/Bcl-2 ratio were decreased significantly as compared with ischemia-reperfusion group.However,the level of Bcl-2 protein was up-regulated in PEP-1-SOD1 groups (P < 0.05,P< 0.01). Conclusion PEP-1-SOD1 can inhibit the cardiomyocyte apoptosis probably through the mechanisms of alleviating oxidative stress,down-regulating Bax and up-regulating Bcl-2 proteins.