雌激素对大鼠肾缺血再灌注损伤后肾叶间动脉舒缩功能及Cx43表达的影响

发布时间：2018-06-17 14:33

本文选题：雌激素 + 肾缺血再灌注损伤　；参考：《西安交通大学学报(医学版)》2017年04期

【摘要】：目的研究雌激素(estrogen,E2)对大鼠肾缺血再灌注损伤后肾叶间动脉缝隙连接蛋白43(connexin43,Cx43)表达的影响。方法建立SD大鼠肾缺血再灌注损伤模型,随机分为正常组、假手术组、缺血再灌注损伤组和E2干预组,于缺血再灌注损伤后24h检测肾功能变化;肾组织切片HE染色行Paller评分,量化肾损害程度。运用压力肌动技术检测各组大鼠肾叶间动脉的舒缩功能。免疫荧光技术、qRT-PCR及Western-blot检测各组大鼠肾叶间动脉Cx43表达的差异。结果 E2能明显降低肾缺血再灌注损伤大鼠血清中血清肌酐(Cr)和尿素氮(BUN)水平,差异有统计学意义(P0.05),且能显著改善肾组织损害程度。肾缺血再灌注损伤后肾叶间动脉收缩率(24.80±3.70)%,给予E2干预后肾叶间动脉收缩率为(41.60±3.50)%,明显高于缺血再灌注损伤组,差异有统计学意义(P0.05)。E2干预组肾叶间动脉上Cx43蛋白的表达水平明显低于缺血再灌注损伤组(P0.01)。结论 E2能够下调缺血再灌注损伤后肾叶间动脉平滑肌细胞Cx43蛋白的表达,抑制缝隙连接(GJ)功能,从而降低血管紧张度,促进血管舒张,有效减轻肾缺血再灌注损伤,改善肾功能。
[Abstract]:Objective to study the effect of estrogen (E2) on the expression of gap connexin 43 (connexin43, Cx43) in the renal interlobular artery after renal ischemia reperfusion injury in rats. Methods the model of renal ischemia reperfusion injury in SD rats was established. The model was randomly divided into normal group, sham operation group, ischemia reperfusion injury group and E2 intervention group, and 24h detection after ischemia-reperfusion injury. Change of renal function, HE staining of renal tissue section, Paller score, quantifying the degree of renal damage. The systolic and diastolic function of renal interlobular artery in each group was detected by pressure muscle technique. Immunofluorescence technique, qRT-PCR and Western-blot were used to detect the difference of Cx43 expression in the interlobular arteries of the rats. The E2 could significantly reduce the renal ischemia reperfusion injury in rats. The serum levels of serum creatinine (Cr) and urea nitrogen (BUN) were statistically significant (P0.05), and could significantly improve the degree of renal tissue damage. The systolic rate of the renal interlobar artery was (24.80 + 3.70)% after renal ischemia-reperfusion injury. The systolic rate of the renal interlobar artery was (41.60 + 3.50)% after E2 intervention, which was significantly higher than that of the ischemia reperfusion injury group. The difference was statistically significant. The expression level of Cx43 protein in the interlobular artery of the.E2 intervention group was significantly lower than that of the ischemia reperfusion injury group (P0.01). Conclusion E2 can reduce the expression of Cx43 protein in the smooth muscle cells of the interlobular artery after ischemia reperfusion injury and inhibit the function of the gap junction (GJ), thus reducing the vascular tensioning, promoting the vasodilatation, and reducing the vasodilatation effectively. Renal ischemia-reperfusion injury, improve renal function.
【作者单位】：石河子大学医学院生理学教研室;石河子大学医学院第一附属医院泌尿外科;
【基金】：国家自然科学基金资助项目(No.81560175,81560081,31260247)~~
【分类号】：R692

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