【摘要】 目的 探究梓醇对卵巢早衰大鼠卵巢功能的保护作用是否与核因子E2相关因子2（Nrf2）/血红素加氧酶1（HO-1）信号通路有关。方法 将大鼠随机分为对照组、模型组、低、中、高剂量梓醇组、高剂量梓醇+ML385组。相应检测试剂盒测定氧化应激水平、血清性激素水平、卵巢组织病理变化、卵巢细胞凋亡、蛋白表达分别采用ELISA法、HE染色、TUNEL法和Western blot法检测。结果 对照组大鼠卵巢呈现正常形态学特征,闭锁卵泡较为罕见,可见各发育阶段的卵泡分布;模型组闭锁卵泡变多,正常卵泡减少;模型组相较于对照组AMH、E₂、SOD水平、Bcl-2、Nrf2、HO-1降低,FSH、ROS、MDA、细胞凋亡率、Cleaved caspase-3、Bax蛋白表达升高（P<0.05）;与模型组相比,低、中、高剂量梓醇组上述指标呈反向改善;与高剂量梓醇组相比,高剂量梓醇+ML385组上述改善趋势被逆转。结论 梓醇可能激活Nrf2/HO-1通路保护卵巢早衰大鼠的卵巢功能。更多还原

【Abstract】 Objective To investigate whether the protective effect of catalpol on ovarian function in premature ovarian failure rats is related to the nuclear factor erythroid 2 related factor 2（Nrf2）/heme oxygenase-1（HO-1） signaling pathway. Methods Rats were randomly divided into control group, model group, low-, medium-, and high-dose catalpol groups, and high-dose catalpol + ML385 group. The level of oxidative stress was determined using corresponding detection kits. Serum sex hormone levels, ovarian histopathological changes, ovarian cell apoptosis, and protein expression were detected by ELISA, HE staining, TUNEL assay, and Western blot, respectively. Results In the control group, the ovaries of rats showed normal morphological characteristics, with relatively rare atretic follicles, and follicles at various developmental stages could be observed; the model group showed an increase in blocked follicles and a decrease in normal follicles. For the control group, the model group showed a decrease in AMH, E₂, SOD, Bcl-2, Nrf2, and HO-1, and an increase in FSH, ROS, MDA, apoptosis rate, Cleaved caspase-3, and Bax（P < 0.05）. Compared with the model group, the low-, medium-, and high-dose catalpol groups showed opposite improvements in the above indicators; compared with the high-dose catalpol group, the improvement trend of the above indicators was reversed in the high-dose catalpol + ML385 group. Conclusions Catalpol may protect ovarian function in rats with premature ovarian failure by activating the Nrf2/HO-1 pathway.更多还原