补充银杏制剂对过度训练大鼠心肌细胞凋亡的影响

Effects of Ginkgo Biloba Exrtact on Cardiomyocyte Apoptosis and Bax,Bcl-2 Gene Expression in Overtrained Rats

目的 :观察银杏制剂对过度训练大鼠心肌细胞凋亡的影响 ,探讨通过干预细胞凋亡而实现对运动心脏的保护作用。方法 :2 4只雄性SD大鼠随机分为 3组 :A组 :安静对照组 (n =8) ;B组 :过度训练组 (n =8) ,递增负荷游泳训练 7周 ;C组 :过度训练 +喂服银杏组 (n =8) ,训练方案同B组 ,同时喂服银杏片 5 0mg/kg/d ,3组大鼠于 7周后取材。采用原位末端标记 (TUNEL)、流式细胞术和免疫组化法分别检测大鼠心肌细胞凋亡及Bcl - 2、Bax基因表达 ,同时检测大鼠血浆和心肌细胞超氧化物歧化酶 (SOD)活性及丙二醛 (MDA)含量。结果 :(1)过度训练对心肌细胞凋亡率的影响 :B组大鼠心肌细胞凋亡率显著高于A组 (P <0 0 5 ) ,C组大鼠心肌细胞凋亡率显著低于B组 (P <0 0 1) ,与A组比较无显著差异。 (2 )与A组相比 ,B组大鼠心肌细胞Bcl- 2蛋白表达显著减弱 ,Bax蛋白表达显著增强 (P <0 0 5 ) ,而C组这两种蛋白的表达与A组均无显著差异。 (3)与A组相比 ,B组大鼠血浆和心肌细胞抗氧化酶SOD活性显著降低 ,脂质过氧化产物MDA显著增加。而C组与A组无显著差异。结论 :银杏制剂可通过其抗氧化作用及影响凋亡相关基因的表达而抑制心肌细胞过度凋亡 ,从而发挥心肌保护作用。

Objective To observe the effects of ginkgo biloba extract(GBE) on apoptosis of cardiomyocyte of overtrained rats and thus to explore the possible protection mechanism of cardiomyocytes damage from excessive exercise. Methods Twenty-four male Sprague-Dauley rats were randomly divided into sedentary control group(Group A,n=8), excessive exercise group(Group B,n=8), excessive exercise+ GBE group (Group C,n=8). The rats in group B and C swam for 7 weeks with incremental intensity. Cardiomyocyte apoptosis,Bax and Bcl-2 genes expression were investigated with TUNEL,flow cytometry and immunohistochemistry techuique. The concentrations of SOD,MDA in plasma and cardiomyocyte were also detected. Results (1) Cardiomyocyte apoptosis ratio in group B had no significant difference from that of group A(P>0.05), but significantly lower than in group B(P<0.01). (2) Bcl-2 gene expression was significontly lower(P<0.05)and Bax was remarkably higher (P<0.05)than in group A, but no significant difference between group A and C was found(P>0.05). (3) Compared with group A, SOD activity of cardiomyocyte and plasma decreased significantly and the contents of MDA increased remarkably in group B.Similarly,There was no significant difference in the indexes between group A and C. Conclusions GBE can prevent cardiomyocyte over-apoptosis via its antioxidation and regulation effects on the expression of bax and bcl-2.