星状神经节阻滞对肾缺血-再灌注大鼠肾组织中Bcl-2和Bax蛋白表达的影响

Effect of stellate ganglion blockade on expression of Bcl-2 and Bax in kidney tissues of ischemia-reperfusion at rats

目的探讨星状神经节阻滞对肾缺血-再灌注大鼠模型肾组织损伤的保护作用及作用机制。方法健康成年SD大鼠30只,随机分为3组,每组10只:假手术组(Sham组)、缺血-再灌注组(IR组)、缺血-再灌注+颈交感神经干离断组(IR+TCST组)。手术后48 h测各组大鼠血肌酐(S_(cr))、尿素氮(BUN)含量及尿量的变化;取大鼠肾组织,观察形态结构变化;westeron blot检测肾组织中Bcl-2和Bax蛋白的表达水平。结果 IR组大鼠血浆中S_(cr)和BUN均明显增高,尿量减少,可见广泛的肾小管上皮细胞发生凋亡,Bcl-2蛋白含量减少而Bax蛋白含量升高,与Sham组相比,差异有统计学意义(P<0.05);IR+TCST组大鼠血浆S_(cr)和BUN均明显降低,尿量增加,肾组织中肾小管上皮细胞凋亡数量减少,Bcl-2蛋白含量升高而Bax蛋白含量减少,与IR组相比,差异有统计学意义(P<0.05)。结论星状神经节阻滞对大鼠肾缺血-再灌注损伤具有保护作用,其机制是通过增加肾组织中Bcl-2蛋白的表达量,降低Bax蛋白的表达水平来抑制肾小管上皮细胞凋亡。

[Objective] To explore the protective effect of stellate ganglion blockade（SGB） on the renal ischemia-reperfusion injury at rats,analyze its mechanism.[Methods]30 healthy adult SD rats were randomly divided into three groups： control group（Sham group）,ischemia-reperfusion（IR）group,ischemia-reperfusion＋transection of cervical sympathetic trunk（IR＋TCST）group,10 rats in each group. 48 hours after operation,the contents of serum creatinine（Scr）and blood urea nitrogen（BUN）and change in urine volume were detected,the morphological structure of kidney tissues in each group were observed,and expression levels of Bcl-2 and Bax in kidney tissues were detected by Westeron blot.[Results]In IR group,the contents of Scrand BUN significantly increased,the volume of urine reduced,there was extensive tubular epithelial cells apoptosis,Bcl-2 protein content decreased while Bax protein content increased,and the differences were statistically significant between IR group and Sham group（P〈0.05）.In IR ＋TCST group,the contents of Scrand BUN significantly increased,the volume of urine increased,the apoptosis number of tubular epithelial cells in kidney tissue decreased,Bcl-2 protein content increased while Bax protein content decreased,and the differences were statistically significant between IR ＋TCST group and Sham group（P〈0.05）.[Conclusion]SGB has protective effect on kidney ischemia-reperfusion injury at rats,is that it can increase the expression level of Bcl-2 and decrease the expression level of Bax to suppress the apoptosis of renal tubular epithelial cell.