Yang Dong-Mei, Zhang Jing-Qin, Fei Yi-Fei
Department of Gynecology, People's Hospital of Linyi City, Shandong, P. R. China.
Department of Gynecology, People's Hospital of Feixian County, Linyi City, Shandong, P. R. China.
J Obstet Gynaecol Res. 2017 Oct;43(10):1621-1628. doi: 10.1111/jog.13416. Epub 2017 Aug 17.
We aimed to examine the effects of Lycium barbarum polysaccharide (LBP) on ovarian damage induced by cyclophosphamide (CTX) and to investigate the underlying mechanism.
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.
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.
LBP exerts protective effects against CTX-induced ovarian injury by reducing oxidative stress and activating the Nrf2/ARE-signaling pathway.
我们旨在研究枸杞多糖（LBP）对环磷酰胺（CTX）诱导的卵巢损伤的影响，并探讨其潜在机制。
将240只雌性Sprague-Dawley大鼠随机分为五组：对照组、CTX诱导的卵巢损伤（OI）组和三个LBP组。对LBP组通过灌胃给予不同浓度的LBP溶液，持续15天，然后OI组和LBP组再接受CTX治疗15天。在注射CTX后的第7、14和28天，采集股静脉血和卵巢组织，用于测量抗氧化酶和氧化产物。通过酶联免疫吸附测定法测量血清指标；通过蛋白质印迹分析检测Nrf2、血红素加氧酶-1和醌氧化还原酶1的蛋白水平。
LBP减轻了CTX诱导的卵巢损伤，并逆转了相关的不良反应。LBP通过增强抗氧化酶的活性和减轻CTX注射后氧化产物水平的升高来降低氧化应激。此外，LBP上调了Nrf2、血红素加氧酶-1和醌氧化还原酶1的蛋白表达。
LBP通过降低氧化应激和激活Nrf2/ARE信号通路，对CTX诱导的卵巢损伤发挥保护作用。
