Dong-Mei Yang1, Jing-Qin Zhang2, Yi-Fei Fei3. 1. Department of Gynecology, People's Hospital of Linyi City, Shandong, P. R. China. 2. Department of Gynecology, People's Hospital of Feixian County, Linyi City, Shandong, P. R. China. 3. Department of Medical Insurance, People's Hospital of Linyi City, Shandong, P. R. China.
Abstract
AIM: We aimed to examine the effects of Lycium barbarum polysaccharide (LBP) on ovarian damage induced by cyclophosphamide (CTX) and to investigate the underlying mechanism. METHODS: A total of 240 female Sprague-Dawley rats were randomly divided into five groups: the control group, the CTX-induced ovarian injury (OI) group, and three LBP groups. Different concentrations of LBP solution were administered to the LBP groups by gastric infusion for 15 days, and the OI group and LBP groups were then subjected to CTX treatment for another 15 days. On days 7, 14, and 28 after CTX injection, femoral vein blood and ovarian tissues were collected for the measurements of antioxidant enzymes and oxidation products. Serum indicators were measured by enzyme-linked immunosorbent assay; and Nrf2, heme oxygenase-1, and quinone oxidoreductase 1 protein levels were detected by Western blot analysis. RESULTS: LBP attenuated CTX-induced ovarian damage and reversed associated adverse effects. LBP reduced oxidative stress by enhancing the potency of antioxidant enzymes and attenuating elevated levels of oxidation products following CTX injection. Furthermore, LBP upregulated Nrf2, heme oxygenase-1, and quinone oxidoreductase 1 protein expression. CONCLUSION: LBP exerts protective effects against CTX-induced ovarian injury by reducing oxidative stress and activating the Nrf2/ARE-signaling pathway.
AIM: We aimed to examine the effects of Lycium barbarum polysaccharide (LBP) on ovarian damage induced by cyclophosphamide (CTX) and to investigate the underlying mechanism. METHODS: A total of 240 female Sprague-Dawley rats were randomly divided into five groups: the control group, the CTX-induced ovarian injury (OI) group, and three LBP groups. Different concentrations of LBP solution were administered to the LBP groups by gastric infusion for 15 days, and the OI group and LBP groups were then subjected to CTX treatment for another 15 days. On days 7, 14, and 28 after CTX injection, femoral vein blood and ovarian tissues were collected for the measurements of antioxidant enzymes and oxidation products. Serum indicators were measured by enzyme-linked immunosorbent assay; and Nrf2, heme oxygenase-1, and quinone oxidoreductase 1 protein levels were detected by Western blot analysis. RESULTS: LBP attenuated CTX-induced ovarian damage and reversed associated adverse effects. LBP reduced oxidative stress by enhancing the potency of antioxidant enzymes and attenuating elevated levels of oxidation products following CTX injection. Furthermore, LBP upregulated Nrf2, heme oxygenase-1, and quinone oxidoreductase 1 protein expression. CONCLUSION: LBP exerts protective effects against CTX-induced ovarian injury by reducing oxidative stress and activating the Nrf2/ARE-signaling pathway.