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探讨前列腺素E1对肾缺血再灌注损伤大鼠内皮细胞Rho/Rho激酶信号通路的影响。建立大鼠IRI模型,将健康Wistar大鼠75只随机平均分为假手术组、模型组、治疗组,每组各25只;并按术后观察时间分为6、12、24、48、72 h 5个不同时段亚组,每组各5只。检测各组血清肌酐(Scr)、血管内皮生长因子(Vas-cular endothelial growth factor,VEGF)在血清中的浓度及在肾组织的表达,检测肾组织髓过氧化物酶(My-eloperoxidase,MPO)活性、RhoA蛋白表达的变化。结果表明:(1)缺血60 min,大鼠血清Scr水平及肾小管坏死评分值均较基线值升高,并于再灌注48 h后达高峰,72 h后下降近基线值。(2)肾组织RhoA、VEGF表达及MPO活性于再灌注后6 h开始升高,12 h达高峰,24 h后开始下降,但均较假手术组明显增加(P<0.05)。(3)PGE1治疗组SCr、RhoA、VEGF表达及MPO活性均明显低于模型组(P<0.05)。RhoA、VEGF表达及MPO活性增加,反映了IRI内皮细胞的损伤程度;PGE1通过“阻断”(off swithch)Rho/Rho激酶信号通路,改善IRI内皮-免疫微环境,减轻肾组织损伤。
To investigate the effect of prostaglandin E1 on Rho / Rho kinase signaling pathway in rat renal ischemia / reperfusion injury. The model of IRI was established in rats. 75 healthy Wistar rats were randomly divided into sham operation group, model group and treatment group with 25 rats in each group. The rats were divided into 6,12,24,48,72 h 5 different time subgroups, each group of 5. The levels of serum creatinine (Scr) and Vas-cular endothelial growth factor (VEGF) in serum and the expression of VEGF in renal tissue were detected in each group. Myeloperoxidase (MPO) Activity, changes in RhoA protein expression. The results showed that: (1) After 60 min of ischemia, Scr level and tubular necrosis score of rats increased from the baseline value, reached the peak at 48 h after reperfusion, and dropped to baseline value after 72 h. (2) The expression of RhoA and VEGF and the activity of MPO in renal tissue began to increase at 6 h after reperfusion, reached the peak at 12 h, and then decreased at 24 h, both of which were significantly higher than that of sham operation group (P <0.05). (3) The expression of SCr, RhoA, VEGF and MPO in PGE1 group were significantly lower than those in model group (P <0.05). The expression of RhoA, VEGF and MPO increased, which reflected the damage degree of IRI endothelial cells. PGE1 could improve IRI endothelial-immune microenvironment and reduce renal tissue injury by “off” the Rho / Rho kinase signaling pathway.