Caulis Sargentodoxae Prescription Inhibits Angiogenesis-related Cytokines in a Rat Endometriosis Model

Background: To determine the efficacy of the Caulis Sargentodoxae prescription, which is an empirical formula of Chinese herbs and has definite curative effects on endometriosis. Methods: The Caulis Sargentodoxae prescription on the growth of ectopic endometria was studied with a rat endometriosis (EMS) model. The EMS model was established by autoplastic transplantation. To study the curative effects of Chinese medicine on EMS in comparison with western medicine, gestrinone and an angiogenesis inhibitor were introduced. The rats were randomly divided into seven groups: normal group, model group, ovariectomized group, gestrinone (western medicine) group, Caulis Sargentodoxae prescription (Chinese medicine) group, apatinib (inhibitor) group, and combination (Chinese medicine + inhibitor) group. After administration for 21 days, the growth inhibitory rates of ectopic endometria in the treatment groups were evaluated, and the levels of vascular endothelial growth factor (VEGF) and VEGF receptor-2 (VEGFR2) were detected by ELISA in the serum and peritoneal fluid, as well as in the ectopic endometrial tissues by real-time polymerase chain reaction and Western blotting. Results: The growth inhibitory rates of ectopic endometria in the treatment groups were significantly higher (P < 0.05). In the Caulis Sargentodoxae prescription group, the levels of angiogenesis-related factors, including VEGF and VEGFR2, were reduced in the serum and peritoneal fluid compared with the model group (P < 0.05). In addition, the positive expression of VEGF and VEGFR2 in ectopic endometria significantly decreased in the Caulis Sargentodoxae prescription group both at mRNA and protein levels. Conclusions: VEGF and VEGFR2 levels in the serum and peritoneal fluid can be used as a clinical reference for endometriotic pathogenesis and treatment, and the Caulis Sargentodoxae prescription has reliable therapeutic effects on EMS for its target-action ability to decrease angiogenesis.