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标题：The effect of gonadotropin-releasing hormone analogues on the preservation of ovarian function against cyclophosphamide-induced damage in adult mice
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作者：Kishk, Eman ; Hassan, Wael ; Shaaban, Mohammed 等
期刊名称：Proceedings in Obstetrics and Gynecology
印刷版ISSN：2154-4751
出版年度：2020
卷号：9
期号：3
页码：1-14
出版社：University of Iowa
摘要：Objective: To assess the effect of gonadotropin-releasing hormone analogue (GnRHa) on the preservation of ovarian function against cyclophosphamide-induced gonadal toxicity. Materials and Methods: In a controlled, experimental study, 64 female mice were divided into four groups: control (C), triptorelin acetate (T), cyclophosphamide (CY), and triptorelin plus cyclophosphamide (T+CY) groups. Mice in the group (T) were subcutaneously injected with GnRHa (triptorelin acetate) in a dose of 0.5 mg/kg daily for 21 days. In contrast, mice in the (CY) group and (T+CY) group were injected intraperitoneally with 75 mg/kg of CY on day 15. After 21 days, half of the mice in each group were sacrificed, and their ovaries were removed. The rest of the mice in each group were left without any intervention for an additional 21 days, and the same procedures were repeated to assess the ovarian follicles. Results: There was signiﬁcant depletion of ovarian follicles in the CY group compared to the control group (p<0.05). There were significant decreases in the number of secondary and antral follicles at late stage as compared to early stage in the CY group (p<0.05). There was also a significant increase in the number of primordial and primary follicles in the T+CY group as compared with the CY group early post-treatment, while the increase was significant in all follicles after 42 days (p<0.05). Conclusion: Cyclophosphamide destroys primordial and primary follicles at an early stage while damage in secondary and antral follicles was prominent after 42 days. Triptorelin acetate reduces the toxic effect of CY; it has early and late protective effects and preserves ovarian function in mice.
关键词：GnRH analogue; cyclophosphamide; ovarian toxicity; ovarian function