【摘要】 目的探讨粉防己碱对缺血-再灌注损伤大鼠心肌细胞凋亡及Bcl-2/Bax蛋白表达的影响。方法结扎大鼠左冠状动脉前降支(LAD)30min后松开,再灌注24h建立心肌缺血-再灌注损伤模型。将48只雄性SD大鼠随机分为:假手术组(Sham组),缺血-再灌注损伤组(IRI组),粉防己碱预处理组(Tet组)。再灌注结束后检测血清肌酸激酶同工酶MB(CK-MB)和心肌梗死范围(IS/AAR,%)。应用原位末端标记法(TUNEL法)检测各组凋亡细胞,计算凋亡指数(AI),应用免疫组化法检测心肌Bcl-2、Bax蛋白表达,计算Bcl-2/Bax值,进行组间比较。结果与IRI组相比,Tet可明显降低CK-MB值(976.57±160.69)vs(1910.38±221.10)U/L,P<0.01,减小心肌IS/AAR%,(23.28±4.38)%vs(43.76±6.30)%,P<0.01。与IRI组比较,粉防己碱预处理可显著减少心肌细胞凋亡,AI显著降低(8.62±2.45%vs19.36±5.28%,P<0.01)。粉防己碱预处理使Bcl-2表达增加,Bax表达下降,Bcl-2/Bax值显著升高(P<0.01)。结论粉防己碱能明显抑制缺血-再灌注损伤引起的心肌细胞凋亡,其作用机制可能与促进Bcl-2蛋白表达,减少Bax蛋白表达、升高Bcl-2/Bax比值有关。更多还原

【Abstract】 Objective To investigate the effect of tetrandrine on cardiomyocyte apoptosis and expression of Bcl-2/Bax protein after ischemia and reperfusion injury in rats. Methods The Sprague-Dawley rats underwent 30 min of left anterior descending(LAD) coronary occlusion and 24 hours reperfusion to make ischemia/repefusion injury(IRI) model in vivo. 48 male rats were randomly divided into 3 groups: Sham group, IRI group, tetrandrine pretreatment group(Tet group). Creatine kianse isoenzyme-MB(CK-MB) was measured in each group, and the infarction size(IS/AAR%) was measured in IRI and Tet groups. The apoptotic index(AI) by TUNEL staining was measured in each group. The protein expression of Bcl-2 and Bax was studied by immunohistochemical staining, and the ratios of Bcl-2 and Bax were calculated. Results Compared with IRI group, the activity of CK-MB in serum was markedly decreased in Tet group[(976.57±160.69) vs (1910.38± 221.10)U/L,P<0.01], the value of IS/AAR% in Tet group was lower than IRI group(23.28±4.38% vs 43.76 ± 6.30%,P<0.01). AI was significantly decreased in Tet group compared with IRI group(8.62±2.45% vs 19.36±5.28%,P<0.01). Compared with IRI group, the expression of Bax protein was decreased significantly and bcl-2 protein was increased significantly in Tet group. The ratios of Bcl-2/Bax in Tet group were significantly increased. Conclusion Tetrandrine can significantly inhibit cardiomyocyte apoptosis induced by ischemia/reperfusion injury in rats. The possible mechanism is to raise the ratio of Bcl-2/Bax proteins by increasing expression of bcl-2 protein and inhibiting expression of Bax protein.更多还原