摘要
目的:观察St.Thomas和河豚毒素(Tetrodotoxin,TTX)两种心脏停搏液对缺血再灌注大鼠心肌细胞凋亡及凋亡相关蛋白表达的影响。方法:Wistar大鼠24只,建立Langendorff-Neely离体心脏灌注模型,分为3组(n=8):对照组、STH-2组、TTX组。用TUNEL法检测心肌细胞凋亡指数(Apoptosis index,AI),免疫组化测定凋亡相关蛋白Bcl-2、Bax、p53的表达,Western blot检测Bcl-2蛋白表达。结果:STH-2组AI(11.20±0.79)%高于TTX组(6.92±1.10)%和对照组(1.34±0.23)%(P<0.01)。TTX组Bcl-2的PEI为(22.63±1.10)%高于STH-2组(13.51±0.67)%和对照组(2.52±0.58)%(P<0.01);STH-2组Bax的PEI为(8.04±0.57)%高于TTX组(6.05±0.46)%和对照组(2.14±0.57)%(P<0.01)。TTX组Bcl-2/Bax为3.78±0.41高于STH-2组1.75±0.15(P<0.01)。TTX组Bcl-2的相对蛋白含量为(86.1±0.98)%高于STH-2组(53.2±1.76)%和对照组(23.7±2.61)%(P<0.01)。p53蛋白在各组均未见明显阳性表达。结论:与STH-2比较,TTX能减少缺血再灌注大鼠心肌细胞凋亡数,其抗凋亡的机制可能与上调Bcl-2表达,下调Bax表达,提高Bcl-2/Bax比值有关。
Objective.To explore the effect of two kinds of cardioplegia on cardiomyocyte apoptosis and the related protein expressions in rat hearts. Methods:24 Wistar rats were randomly divided into 3 groups (n=8):Control group,STH-2 group and TTX group. Isolated rat Langendorff and Neely working heart models were estabished. The changes in cardiomyocyte apoptosis were detected by TUNEL. The expression of Bcl-2 and Bax protein were detected by immunohistochemical assay in cardiomyocyte. The expression of Bcl-2 protein in cardiomyocyte was detected by Western blot. Results:Apoptosis index(AI) in STH-2 group ( 11.20 ± 0.79 ) % was significantly higher than that in TTX group (6.92 ± 1.10) % and Control group ( 1.34 ± 0.23 ) % (P〈0.01). Bcl-2 protein expression index(PEI) in TTX group(22.63 ±1.10)% increased as compared with STH-2 group (13.51±0.67)% and Control group (2.52 ±0.58)%(P〈0.01). Bax PEI in STH-2 group (8.04±0.57)%increased as compared with TTX group (6,05 ±0.46)% and Control group (2.14 ±0.57)%(P〈0.01). Bcl-2/Bax was 3.78 was 0.41 in TTX group,1.75 ±0.15 in STH-2 group. Bcl-2 protein expression in TTX group (86.1 ±0.98)% increased as compared with STH-2 group (53.2± 1.76)% and Control group (23.7 ±2.61)%(P〈0.01 ). There was no sign of p53 protein expression in all groups. Conclusion:Compared with STH-2,TTX cardioplegia alleviates the apoptosis of rat cardiomyocytes. The mechanism is probably up-regulating expression of Bcl-2 protein,down-regulating expression of bax protein and increasing Bcl-2/Bax.
出处
《重庆医科大学学报》
CAS
CSCD
2008年第9期1047-1049,1070,共4页
Journal of Chongqing Medical University
基金
重庆市科委课题(CSTC
2005AC0068)