贝前列腺素钠对梗阻性肾病再通大鼠的疗效及机制研究

Research for therapeutic effects and mechanism of beraprost sodium in rat with obstructive nephropathy

目的:研究贝前列腺素钠对梗阻性肾病再通大鼠的保护作用及机制。方法:通过单侧输尿管结扎手术建立梗阻性肾病大鼠模型,将大鼠分为假手术组、模型组和贝前列腺素钠治疗组三组,术后第15天处死大鼠,收集血清检测肌酐、尿素氮、血钠和血钾的水平,苏木精-伊红(HE)染色评价肾组织损伤程度,Western blot检测大鼠肾组织肾损伤分子1(KIM-1)、缺氧诱导因子α(HIF-α)和转化生长因子β(TGF-β)蛋白表达水平。结果:模型组大鼠血清肌酐、尿素氮和血钾的含量显著高于假手术组,血钠的含量显著低于假手术组(P<0.05)。贝前列腺素钠治疗组大鼠血清肌酐、尿素氮和血钾的含量显著低于模型组,血钠的含量显著高于模型组(P<0.05)。HE染色结果显示,与模型组比较,贝前列腺素钠治疗组的肾组织损伤程度显著降低。Western blot检测结果显示,与模型组比较,贝前列腺素钠治疗组的肾组织KIM-1、HIF-α和TGF-β蛋白表达水平显著降低。结论:贝前列腺素钠能够改善梗阻性肾病梗阻解除后的肾损伤,抑制肾脏中TGF-β、HIF-α和KIM-1的表达。

Objective:To explore the therapeutic effects and mechanism of beraprost sodium in rat with obstructive nephropathy.Method:The obstructive nephropathy rat model was established by unilateral ureteral ligation.The rats were divided into 3 groups,sham operation group,model group and beraprost sodium treatment group.The rats were sacrificed on the 15 th day after operation.The levels of Scr,BUN,serum sodium and potassium were detected.The degree of renal injury was evaluated by HE staining.The expressions of KIM-1,HIF-αand TGF-βprotein in rat kidney were detected by Western blot.Result:The levels of Scr,BUN,and serum potassium in the model group were significantly higher than those in the sham operation group.The serum sodium content was significantly lower than that in the sham operation group(P<0.05).The levels of Scr,BUN,and serum potassium in the beraprost sodium treatment group were significantly lower than those in the model group.The serum sodium content was significantly higher than that in the model group(P<0.05).The results of HE staining showed that the degree of renal tissue damage was significantly lower in the beraprost sodium treatment group than that in the model group.Western blot analysis showed that compared with the model group,the expression levels of KIM-1,HIF-αand TGF-βprotein in renal tissue of beraprost sodium treatment group were significantly lower.Conclusion:Beraprost sodium can alleviate renal damage induced by obstructive nephropathy and inhibit the expression of TGF-β,HIF-αand KIM-1 in renal tissues.