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G蛋白偶联雌激素受体通过减轻大鼠肾小管上皮细胞凋亡保护肾脏缺血再灌注损伤
GPER protects renal ischemia-reperfusion injury by reducing the apoptosis of renal tubular epithelial cells in rats
【摘要】 目的探讨G蛋白偶联雌激素受体(G protein-coupled estrogen receptor,GPER)能否减轻肾小管上皮细胞凋亡,从而保护肾脏缺血再灌注(ischemia-reperfusion,I/R)损伤。方法雌性去卵巢(ovariec-断剂)+G1组。检测各组大鼠肾功能,HE染色、Paller评分评价肾组织损伤程度,观察肾组织凋亡相关蛋白(P <0.01),Bcl-2蛋白在肾小管上皮细胞阳性表达及肾组织的表达均减少,Caspase-3蛋白在肾小管上皮细0.01),Bcl-2蛋白的表达上升,Caspase-3蛋白的表达下降(P <0.01);G15组可部分逆转G1激活GPER后的现的。
【Abstract】 Objective To investigate the effect of G protein-coupled estrogen receptor (GPER) on ischemia-reperfusion(I/R)injury.Method s Female ovariectomized(OVX)rats were randomly divided into OVX group,OVX+I/R group,OVX+I/R+G1(GPER agonist)group,OVX+I/R+G15(GPER blocker)+G1group.The renal function of rats in each group was detected,HE staining and Paller score were used to evaluate the degree of renal tissue damage,and the expression position and expression level of renal tissue apoptosisrelated proteins were observed.Results Compared with the OVX group,the renal function of the OVX+I/R group was significantly damaged(P<0.01),Paller score increased(P<0.01),and the positive expression of Bcl-2protein in renal tubular epithelial cells and the expression of renal tissue were reduced.The positive expression of Caspase-3 protein in renal tubular epithelial cells and the expression of renal tissue increased(P<0.01).The renal function damage was significantly reduced after G1 intervention (P<0.01),Paller score significantly decreased(P<0.01),the expression of Bcl-2 significantly increased,and the expression of Caspase-3 protein significantly decreased (P<0.01).The protective effect of G1 activated GPER G15 group was partially reversed(all P<0.01).Conclusion Activated GPER can alleviate renal I/R injury,and its mechanism may be achieved by regulating the apoptosis pathway.
【Key words】 G protein-coupled estrogen receptor; renal ischemia-reperfusion injury; renal tubular epithelial cells; apoptosis;
- 【文献出处】 实用医学杂志 ,The Journal of Practical Medicine , 编辑部邮箱 ,2021年10期
- 【分类号】R692
- 【被引频次】6
- 【下载频次】271