Effects of Kidney-Supplementing Yang-Warming Stasis-Removing Formula on BK /BKB1R and PGF2α in Mice With Endometriosis

Objective To study the mechanism of Kidney-Supplementing Yang-Warming Stasis-Removing Formula( KYSF) for dysmenorrhea caused by endometriosis.Methods Totally 75 male BALB / c mice were randomized into the sham operation group,model group,KYSF high-dose group,KYSF low-dose group and western medicine group,with 15 in each.The mouse models of dysmenorrhea caused by endometriosis were established with surgical transplantation in all groups except the sham operation group.During modeling,the KYSF high-dose group and KYSF low-dose group were given 61.67 g / kg KYSF + 0.5 mg / kg estradiol valerate or 15.42 g / kg KYSF + 0.5 mg / kg estradiol valerate once daily respectively,and the western medicine group was given 0.4 mg / kg gestrinone + 0.5 mg / kg estradiol valerate twice weekly.On the 12th day of modeling,the writhing response and ectopic foci volume was observed,and the contents of bradykinin( BK) and prostaglandin F2α( PGF2α),the expressions of BKB1R protein and BKB1R mRNA in the uterus,and ectopic foci were detected after intraperitoneal injection of oxytocin.Results On the 12th day of modeling,the writhing response and ectopic foci could be seen in all groups except the sham operation group.Comparing with the model group,the latency of writhing was significantly prolonged,writhing times were significantly reduced,and the volume of ectopic foci was significantly decreased in the KYSF groups and western medicine group( P 0.05 or P 0.01).Comparing with the model group,the contents of BK and PGF2α were significantly decreased,and the expressions of BKB1R protein and BKB1R mRNA in the uterus and ectopic foci were significantly decreased in the KYSF groups and western medicine group( P 0.01).Also,the expression of BKB1R mRNA in the KYSF high-dose group was significantly lower than that in the western medicine group( P 0.01).Conclusion KYSF can effectively prevent and treat endometriosis,which may be associated with decreasing the contents of BK and PGF2α and inhibiting the expressions of BKB1R protein and BKB1R mRNA.