丙泊酚对肾缺血-再灌注损伤大鼠肾叶间动脉缝隙连接Cx43表达的影响

摘要

Objective To observe the effects of propofol intervention on renal ischemia-reperfusion injury on the expression of Cx43 in rat renal interlobar artery.Methods Male SD rats were randomly divided into control 4h and 24h groups (control), sham operation 4h and 24h groups (sham), ischemia reperfusion 4h and 24h groups (I/R), propofol 4h and 24h groups (propofol), and fat emulsion 4h and 24h groups (intralipid).Ischemia/reperfusion model was prepared by resection of right kidney and noninvasive arterial occlusion of left kidney, with renal ischemia for 45min and reperfusion for 4h or 24h depending on different group.Serum urea nitrogen (BUN) and creatinine (Cr) were detected by automatic biochemical analyzer.HE staining was used to observe the pathological changes of renal tissue.The changes of renal artery systolic and diastolic lobes were examined by pressure myographic technique.The expression of Cx43 protein in renal interlobar artery was analyzed by Western blot.Results The concentrations of serum BUN and Cr in sham group did not differ significantly from those in the blank control group.Renal HE staining showed no significant lesions;the pressure myogram of motor renal interlobar artery contraction rate showed no significant difference.The expression of Cx43 protein did not change significantly.Compared with sham operation group, the concentrations of serum BUN and Cr in ischemia-reperfusiongroup were significantly increased.HE slices kidney showed that the pathological changes of renal tissue became obvious;pressure motor indicated renal interlobar artery contraction rate was decreased;the expression of Cx43 protein was increased significantly (P<0.05).Compared with ischemia-reperfusion group, the concentrations of serum BUN and Cr in propofol group were decreased;renal HE slices showed reduced renal tissue lesions, increased renal interlobar artery contraction rate, and decreased expression of Cx43 protein (P<0.05).Conclusion Propofol can change renal ischemia-reperfusion injury by reducing the expression of Cx43 protein in vasomotor in renal interlobar artery.%目的 观察丙泊酚干预对肾缺血再灌注损伤大鼠肾叶间动脉(RIA)Cx43表达的影响.方法 雄性SD大鼠随机分为空白对照(control)4h、24h组,假手术(sham)4h、24h组,肾缺血再灌注(I/R)4h、24h组,丙泊酚干预(propofol)4h、24h组,脂肪乳剂(intralipid)4h、24h组.采用切除右肾、无创动脉夹夹闭左肾制备肾缺血再灌注模型,肾缺血45min,按分组不同分别再灌注4h、24h;采用全自动生化仪检测血清尿素氮(serum urea nitrogen, BUN)和肌酐(creatinine, Cr);HE染色法观察肾组织的病理学变化;压力肌动图技术观察RIA收缩舒张的变化;Western blot方法检测RIA Cx43蛋白的表达.结果 与空白对照组相比,假手术组血清BUN、Cr浓度无统计学差异,肾HE染色未发现明显的形态学改变,压力肌动图观察RIA收缩率无统计学差异,Cx43蛋白表达无统计学差异;与假手术组相比,肾缺血再灌注组血清BUN、Cr浓度均显著增高,肾HE切片显示肾组织病变明显,压力肌动图显示RIA收缩率下降,Cx43蛋白表达显著增高,差异有统计学差异(P<0.05);与肾缺血再灌注组相比,丙泊酚干预组血清BUN、Cr浓度有所降低,肾HE切片显示肾组织病变减轻,RIA收缩率有所升高,Cx43蛋白表达降低,差异有统计学意义(P<0.05).结论 丙泊酚可能通过降低RIA Cx43蛋白的表达改变血管舒缩性,从而减轻肾缺血再灌注损伤.