标题：Ginsenoside Rf alleviates dysmenorrhea and inflammation through the BDNF-TrkB-CREB pathway in a rat model of endometriosis
作者：Qin, Xuying; Liu, Yan; Feng, Yanchong; Jiang, Jie
作者机构：[Qin, Xuying; Jiang, Jie] Shandong Univ, QiLu Hosp, Dept Obstet & Gynecol, 104 Culture West Rd, Jinan 250012, Shandong, Peoples R China.; [Qin, Xuyi 更多
通讯作者：Jiang, Jie;Jiang, J
通讯作者地址：[Jiang, J]Shandong Univ, QiLu Hosp, Dept Obstet & Gynecol, 104 Culture West Rd, Jinan 250012, Shandong, Peoples R China.
来源：FOOD & FUNCTION
摘要：To investigate the effects and the underlying mechanisms of ginsenoside Rf in a surgically induced rat endometriosis model, endometriosis was constructed through homologous transplantation and the Wistar rats were further randomly classified into the sham group, the estradiol valerate (E2V) control group, the endometriosis group, and the ginsenoside Rf groups (1.0, 2.0 and 4.0 mg kg(-1), respectively). After 7 days of treatment, the implant volume and writhing responses were recorded. Vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), interleukin (IL)-6, IL-1 beta, and tumor necrosis factor (TNF)-alpha were analyzed using enzyme-linked immunosorbent assay (ELISA) and reverse transcription polymerase chain reaction (RT-PCR) assay. Brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinases (TrkB), and phosphate-c-AMP-responsive element binding protein (pCREB) were further measured. Compared with the endometriosis group, ginsenoside Rf could decrease the volume of the endometriotic implants and writhing responses. Furthermore, the expression levels of VEGF and inflammation-related iNOS, IL-6, IL-1 beta, and TNF-alpha were significantly down-regulated in the ginsenoside Rf groups in a dose-dependent manner. The results also showed that ginsenoside Rf could decrease the expression of BDNF, TrkB, and pCREB in the endometriotic implants. The alleviation of endometriosis-associated dysmenorrhea and inflammation by ginsenoside Rf may be partially mediated by the BDNF-TrkB-CREB pathway.