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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(P<0.05),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(P<0.05)。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(P<0.01)。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。
Objective To study the effect of estrogen on the expression of connexin43 (Cx43) in renal ischemia-reperfusion injury in rats. Methods The model of renal ischemia reperfusion injury in SD rats was established and randomly divided into normal group, sham operation group, ischemia-reperfusion injury group and E2 intervention group. Renal function was detected 24h after ischemia-reperfusion injury. Renal tissue sections HE staining Paller score, quantify the extent of renal damage. The pressure-motor technique was used to detect the systolic and diastolic function of the interrenal artery in rats. Immunofluorescence, qRT-PCR and Western-blot were used to detect the expression of Cx43 in renal interstitial artery of rats in each group. Results E2 significantly decreased serum creatinine (Cr) and blood urea nitrogen (BUN) levels in rats with renal-ischemia-reperfusion injury, with statistical significance (P <0.05) and significantly improved renal damage. The renal interstitial artery contraction rate was (24.80 ± 3.70)% after renal ischemia-reperfusion injury. The contraction rate of intermuscular artery was (41.60 ± 3.50)% after E2 intervention, which was significantly higher than that of ischemia-reperfusion injury group Statistical significance (P <0.05). The expression of Cx43 in the interrenal artery of E2 intervention group was significantly lower than that in ischemia / reperfusion injury group (P <0.01). Conclusion E2 can down-regulate the expression of Cx43 protein in the mesangial artery smooth muscle cells after ischemia-reperfusion injury, inhibit the function of gap junction (GJ), reduce the tension of blood vessels, promote vasodilation, reduce renal ischemia-reperfusion injury and improve renal Features.