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目的观察肾组织Intermedin(IMD)及其受体系统——降钙素受体样受体(CRLR)以及受体活性修饰蛋白(RAMPs)在大鼠肾脏缺血再灌注损伤中的改变。方法用动脉夹夹闭大鼠左侧肾蒂1 h再离体灌注1 h,制成急性肾缺血再灌注损伤动物模型,光镜下观察肾组织形态学变化;放射免疫法测定正常和损伤肾脏IMD含量;半定量RT-PCR测定IMD、CRLR、RAMP1、RAMP2和RAMP3 mRNA水平。结果形态学显示肾缺血再灌注组肾小球结构异常,细胞坏死、混浊肿胀或凋亡,基底膜剥脱;肾脏IMD含量较对照组低63.5%(P<0.01);IMD、CRLR、RAMP1和RAMP3 mRNA分别较对照组低51.8%、60.5%、88.8%和78.8%(P<0.01),而RAMP2 mRNA相对含量与对照组比较无统计学差异。结论缺血再灌注损伤大鼠肾组织IMD生成减少,IMD、CRLR和RAMP1,RAMP3基因表达均降低。提示IMD及其受体系统可能在肾脏缺血再灌注损伤中发挥重要的作用。
OBJECTIVE: To observe the changes of Intermedin (IMD) and its receptor system - calcitonin receptor-like receptor (CRLR) and receptor activity modifying protein (RAMPs) in renal ischemia-reperfusion injury in rats. Methods The left renal pedicle of rats was occluded for 1 h with artery clip for 1 h, then the animal model of acute renal ischemia-reperfusion injury was established. The morphological changes of renal tissue were observed under light microscope. The normal and injury were determined by radioimmunoassay Kidney IMD content; semi-quantitative RT-PCR determination of IMD, CRLR, RAMP1, RAMP2 and RAMP3 mRNA levels. RESULTS: The morphological changes of glomerular structure, necrosis, swollen or apoptotic basement membrane and basement membrane were observed in renal ischemia-reperfusion group. The IMD content in kidneys was 63.5% lower than that in control group (P <0.01) RAMP3 mRNA was 51.8%, 60.5%, 88.8% and 78.8% lower than that of the control group respectively (P <0.01), while the relative content of RAMP2 mRNA was not significantly different from that of the control group. Conclusion The IMD generation, the expression of IMD, CRLR, RAMP1 and RAMP3 in renal tissue of rats with ischemia-reperfusion injury were decreased. Suggesting that IMD and its receptor system may play an important role in renal ischemia-reperfusion injury.