miR-138在肾脏缺血再灌注损伤中的作用及其机制

目的 观察miR-138在肾脏缺血再灌注损伤中的作用及其机制。方法 60只成年SD大鼠，随机分为假手术组（Sham组）、RIRI组、RIRI+空载体（vector）组、RIRI+miR-138（miR-138）组、RIRI+miR-138 shRNA（sh miR-138）组，每组15只，通过夹闭双侧肾蒂建立肾脏缺血再灌注组损伤模型。采用检测血清中肌酐、尿素氮比较各组肾功能差异、Tunel染色检测细胞凋亡、荧光定量PCR检测p53及下游基因变化等方法研究miR-138对肾脏缺血再灌注损伤的作用及其机制。结果 与假手术组比较，缺血再灌注组的肾脏功能BUN、Cr水平，凋亡水平均显著升高，差异有统计学意义（P<0.05）。上调miR-138后，以上指标均显著升高，且差异有统计学意义（P<0.05），下调miR-138则保护肾脏缺血再灌注损伤；进一步研究发现miR-138可能通过抑制p53信号通路发挥作用。结论 miR-138对大鼠肾脏缺血再灌注损伤具有明显的加重作用，其机制可能与p53信号通路密切相关。

Role of miR-138 in the Renal Ischemic Reperfusion Injury and Its Mechanism

Objective To determine the effect of miR-138 on SD rat renal ischemia-reperfusion injury its mechanism. Methods 60 adult SD rats were randomly divided into Sham group, renal ischemia-reperfusion (RIRI) group, RIRI +vector group, RIRI+miR-138 group, RIRI+ miR-138 shRNA group,and then we established renal reperfusion injury model by occlusion bilateral renal pedicle. Creatinine, blood urea nitrogen in serum are tested to compare differences in renal function in each group, and TUNEL staining was taked to detect apoptosis,real time PCR were taked to test the exression of p53 and it''s pathway. Results When compared with the sham group, expression of kidney function BUN/Crin serum, percentage of apoptoiscells of reperfusion injury group wrer all increased, and the differences were statistically significant (P<0.05). Upregulate miR-138 increased these indexes, and the difference was statistically significant (P<0.05), and down regulate miR-138 would protect the injure of renal ischemia-reperfusion. Further studies showed that miR-138 may play the role by inhibiting the p53 signaling pathway. Conclusion MiR-138 has a significant aggravating effect on renal ischemia-reperfusion injury,and the mechanism may be related to p53 signaling pathway.