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.