促红细胞生成素对缺血再灌注损伤大鼠肾脏水通道蛋白2表达的影响

目的 观察促红细胞生成素(EPO)对缺血再灌注损伤(IR)大鼠肾脏水通道蛋白(AQP2)表达的影响,以探讨EPO对IR的保护作用.方法 制备大鼠肾IR模型,将Wistar大鼠随机分为假手术组、肾IR组及EPO治疗组,通过免疫组化、聚合酶链反应及Wostem印迹等方法 ,检测肾组织中AQP2及其mRNA的变化,同时检测肾功能及尿量、尿渗透压的改变和肾组织形态学变化.结果 EPO治疗组肾脏中AQP2及其mRNA的变化、肾功能血肌酐(51±5)μmol/L]及尿量(26.0±2.3)μl·min-1·kg-1]、尿渗透压(1508±121)mOsm/kg H2O]和肾组织形态学变化与肾IR组血肌酐(141±5)μmol/L、尿量(59.1±1.3)μl·min-1·kg-1,尿渗透压(235±99)mOsm/kg H2O]相比均有明显改善(均P<0.05).结论 EPO可以促进IR大鼠肾脏AQP2表达,EPO具有改善大鼠肾脏IR的作用,EPO促进AQP2表达这一机制可能参与了其改善大鼠肾脏IR作用.

Effects of erythrapoietin on the expression of aquaporin-2 after renal ischemia-reperfusion injury: experiment with rats

Objective To investigate the effects of erythropoietin (EPO) on the expression of aquaporin 2 (AQP2) after renal ischemia/reperfusion (IR). Methods Twenty-four Wistar rats were randomly divided into 3 equal groups: IR group undergoing resection of the right kidney, closuring of the left renal artery, vein, and ureter, and un-closuring 40 min later; IR + EPO group undergoing the above mentioned procedures and then intraperitoneal injection of EPO 3000 U/kg on days 1 and 2 after the treatment; and control group undergoing resection of the right kidney only without IR of the left kidney.Urine volume and urine osmotic pressure were measured. Blood samples were collected to detect the serum blood urea nitrogen (BUN) and creatinine (Cr). Three days after the treatment the kidneys were taken out.RT-PCR and Western blotting were used to detect the mRNA and protein expression of AQP2. Results The group was (1508±121) mOsm/kg H2O, significantly higher than that of the IR group (235±99) mOsm/ kg H2O, P<0.01]. The serum BUN and Cr levels of the IR + EPO group were (12.3±6.0) mmol/L and (51±5)μmol/L respectively, both significantly lower than those of the IR group (29.9±3.7) mmol/L and (141±5)μmol/L respeetivdy, both P<0.01]. The mRNA and protein expression of AQP2 were highly positive in the control group. The protein expression levels of AQP2 of the IR + EPO group were not significandy different from those of the control group (both P>0.05), and the protein expression levels of AQP2 of the IR group were significandy lower than those of the control group (both P<0.01). Conclusion EPO can inhibit the down-regulation of AQP2 in response to IR and this may take part in the FRO protective mechanism of renal ischemia/reperfusian injury.