Protective Effects Of Notoginsenoside R1 On Renal Ischemia-Reperfusion Injury In Rats

Objection:To investigate the effect of Notoginsenoside R1 on rat model of renal ischemia-reperfusion injury and the effect of Wntl gene,Frz gene and ?-catenin gene expression on Writ/?-catenin signaling pathway.Methods:In this study,75 healthy male SD rats were randomly divided into 5 groups:sham group(Sham group),ischemia reperfusion group(IRI group),5mg/kg administration group of notoginsenoside R1(IRI+ group),10mg/kg administration group(IRI + 10 group)and 15mg/kg administration group(IRI+ 15 group),and each group of 15.IRI group and notoginsenoside R1 administration group were used to prepare rat renal ischemia-reperfusion injury model by clipping right renal artery.Sham group only exposed the right renal artery but not to be clipped.The rats in the administration group were injected with different concentrations of notoginsenoside RI,sham group and the IRI group were injected with equal volume of normal saline.Kidney samples were taken at 0h,12h,24h,48h and 72h after ischemia-reperfusion.The pathological changes of renal tubules were observed by HE staining.The expression of Wntl gene,Frz gene and ?-catenin gene were detected by real-time PCR.The expression of Wntl protein,Frz protein and ?-catenin protein was detected by Western blot.Results:(1)Kidney pathology observation showed that:? In the sham group,there was no obvious pathological damage in the kidney of the Sham group.The renal pathological damage of the IRI group was gradually increased and reached the maximum at 24 hours.The pathological damage of the kidney was gradually reduced.With the prolongation of time,the kidney showed different degree of pathological damage,indicating that the experimental rat renal ischemia-reperfusion injury model was successfully prepared.? Compared with IRI group.the renal tubular injury of IRI + 15 group was significantly decreased at 24 hours,48 hours and 72 hours(P<0.05).(2)Real-time PCR results showed that:? The mRNA expression of Wntl,Frz and ?-catenin genes increased gradually with the prolongation of time,while the expression of Wntl and ?-catenin gene reached the maximum at 48h,and then decreased gradually.The mRNA expression of Sham group was not significant.? Compared with IRI group,the renal tubular injury of IRI + 15 group was significantly decreased at 24 hours,48 hours and 72 hours(P<0.05).The mRNA expression of Wntl gene in IRI + 10 group was significantly higher than that in IRI group at 24 h.48 h and 72 h(P<0.05).? Compared with IRI group,the mRNA expression of Frz gene in IRI + 15 group was significantly increased at 24h,48h and 72h(P<0.05).At 48 h,the expression of Frz gene in IRI +10 group was significantly higher than that in IRI group(P<0.05).? Compared with IRI group,the expression of ?-catenin mRNA in IRI +15 group was significantly increased at 24h,48h and 72h(P<0.05).The expression of ?-catenin mRNA in IRI + 10 group was significantly higher than that in IRI group at 48h and 72h(P<0.05).(3)Western blot results showed that:? The expression of Wntl,Frz and ?-catenin increased gradually with the prolongation of time,while the expression of Wntl and P-catenin reached the maximum at 48h,and then decreased gradually.The expression of Wntl,Frz and P-catenin protein in Sham group had no significant change.? Compared with IRI group,the expression of Wntl protein in IRI + 15 group was significantly increased at 24h,48h and 72h(P<0.05).The expression of Wntl protein in IRI +10 group was significantly increased at 48 h and 72 h(P<0.05).At 72 h,the expression of Wntl protein in IRI +5 group was significantly increased(P<0.05).? Compared with IRI group,the expression of Frz and ?-catenin protein in IRI +15 group was significantly increased at 24h,48h and 72h(P<0.05).The expression of Frz and ?-catenin protein in IRI +10 group was significantly increased at 48 h and 72 h(P<0.05).Conclusion:(1)Notoginsenoside R1 can reduce renal ischemia-reperfusion injury in rats.(2)Notoginsenoside R1 protects against renal ischemia-reper-fusion injury in rats by promoting the expression of Wnt gene,Frz gene and ?-catenin gene.