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目的:探讨银杏黄酮(GBE)对顺铂(c DDP)所致人卵巢颗粒细胞功能损伤的保护作用及其机理。方法:将10μg/ml c DDP与不同浓度(0、175μg/L、200μg/L、225μg/L、325μg/ml)GBE同时作用于人卵巢颗粒细胞48h,并设空白对照组。MTT法观察人卵巢颗粒细胞的生长情况;化学发光法测定颗粒细胞上清液E2水平;黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)的活性,硫代巴比妥酸法(TBA法)测定颗粒细胞丙二醛(MDA)含量。结果:空白对照组的细胞呈梭形紧密连接,排列较规则;c DDP组的细胞数明显较少,排列不规则;c DDP+GBE组的细胞较c DDP组增多,部分贴壁。随着GBE浓度(0、175μg/L、200μg/L、225μg/L)的增加,卵巢颗粒细胞的增殖指数、E2水平、SOD活性均增加,MDA含量则减低,差异均有统计学意义(P<0.05)。结论:适量的GBE在体外能减少顺铂所致的人卵巢颗粒细胞损伤、提高雌二醇水平,其机理可能是通过增加SOD活性、降低MDA含量达到对颗粒细胞的保护作用。GBE有望成为保护化疗所致人卵巢损伤的一种理想新药。
Objective: To investigate the protective effect of ginkgetin (GBE) on functional damage of human ovarian granulosa cells induced by cisplatin (c DDP) and its mechanism. Methods: Human ovarian granulosa cells were treated with 10 μg / ml cDDP and GBE at different concentrations (0,175μg / L, 200μg / L, 225μg / L and 325μg / ml) for 48 hours. The growth of human ovarian granulosa cells was observed by MTT assay. E2 level of granulocyte supernatant was determined by chemiluminescence assay. The activity of superoxide dismutase (SOD) was measured by xanthine oxidase method. The activity of thiobarbituric acid ) To determine the content of malondialdehyde (MDA) in granulosa cells. Results: The cells in the blank control group were spindled tightly and arranged regularly. The number of cells in cDDP group was less and arranged irregularly. The number of cells in cDDP + GBE group was more than that in cDDP group, and was partially adherent. With the increase of GBE concentration (0,175μg / L, 200μg / L, 225μg / L), the proliferation index, E2 level and SOD activity of ovarian granulosa cells increased, while the MDA content decreased, the differences were statistically significant <0.05). CONCLUSION: The proper amount of GBE can reduce cisplatin-induced human ovarian granulosa cell damage and increase the estradiol level in vitro. The mechanism may be that the protective effect of GBE can be achieved by increasing the activity of SOD and decreasing the content of MDA. GBE is expected to become an ideal new drug for protecting chemotherapy-induced human ovarian damage.