热休克蛋白27在缺血后处理肾组织中的表达及意义

目的 观察热休克蛋白27（HSP27）在缺血后处理（IPO）肾组织中的表达及分布情况,探讨其在肾缺血后处理中的作用.方法 结扎右侧肾蒂,夹闭左侧肾蒂60 min、再灌注24 h制备肾缺血/再灌注损伤模型.雄性SD大鼠24只,随机分为假手术组（S组）、缺血/再灌注组（I/R组）、缺血后处理组（IPO组）,每组8只.再灌注24 h后处死大鼠,腹主动脉取血并切取左肾.测定血清肌酐（Cr）、尿素氮（BUN）浓度;光镜下观察肾组织病理学改变;免疫组织化学方法检测肾组织中HSP27的表达;TUNEL法检测肾小管上皮细胞凋亡指数（AI）.结果 与S组比较,I/R组Cr和BUN浓度显著升高,组织损伤明显,肾组织中HSP27表达增多,肾小管上皮细胞凋亡指数较高（P〈0.05）;与I/R组比较,IPO组Cr和BUN浓度显著降低,组织损伤较轻,HSP27表达进一步增强,肾小管上皮细胞凋亡指数较低（P〈0.05）.结论 肾缺血后处理能上调肾组织中HSP27的表达,抑制肾小管上皮细胞凋亡,继而减轻肾缺血/再灌注损伤.

The expression and potential effect of HSP27 on renal ischemic postconditioning in rats

Objective To investigate the expression and potential effect of the heat shock protein 27 （ HSP27 ） on renal ischemic postconditioning in rats. Methods The ischemia/reperfusion injury model was established by occlusion of left renal pedicel for 60 min followed by 24 h reperfusion in a right renal pedicel - ligated rat. 24 male SD rats were ran-domly divided into three groups （n = 8 each） ： sham operation （S） group, ischemic/reperfusion （I/R） group and ische-mic postconditioning （IPO） group. After a 24 h reperfusion, the rats were killed with the blood sample taken from ab-dominal aorta and the left renal tissues collected. Blood urea nitrogen （BUN） and creatinine （Cr） concentrations were measured. Moreover, the ischemic left renal tissue was collected for morphological observation using microscope. The ex-pression of HSP27 was detected by immunohistochemistry. In addition, renal apoptosis index （AI） in the renal tubular epithelial cells was assayed by TUNEL. Results Compared with group S, the serum Cr and BUN concentrations and AI were significantly increased, with a significant up - regulation of the expression of HSP27 in I/R group and IPO group （P 〈 0.05）. However, compared with those in I/R group, the serum Cr and BUN concentrations and AI were decreased signifi-cantly （P 〈 0.05）, and the expression of HSP27 was up - regulated in group IPO. Moreover, the microscopic examination showed that the renal I/R injury was significantly attenuated by ischemic postconditioning and the degree of injury in group IPO was similar to that in IFR group. Conclusion Ischemic postconditioning can prevent the renal ischemia/reperfusion injury by up - regulating the expression of HSP27 and inhibiting the apoptosis of renal tubular epithelial cell.