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Journal Article
Research Support, Non-U.S. Gov't
A mouse model of premature ovarian insufficiency induced by tripterygium glycoside via subcutaneous injection.
Premature ovarian insufficiency (POI) is a main cause of infertility and affects nearly 1% women under 40 years old. This study was aimed to utilize the side effects of tripterygium glycoside (TG) to induce a mouse model of POI. 48 female KM mice were divided into four groups: control, oral, intraperitoneal injection and subcutaneous injection group. The mice in last three groups were treated with TG (50 mg•kg(-1)) daily for 35 days, while the mice in control group were treated with parallel volume of sterile water. Vaginal smears were taken to monitor the estrous cycles and estrous frequency for the last 21 days. Ovarian and uterine index and histomorphological change were determined when finished the administration. Serum levels of FSH were assessed by ELISA. Ki-67 expression in the uterus was analyzed from using immunohistochemical detection. And the apoptosis of follicle cells were detected by TUNEL assay. The results showed that mice in subcutaneous injection group presented the critical manifestations with significantly prolonged estrous cycles, decreased estrous frequency, reduced ovarian and uterine index, and increased serum FSH levels. At this dose level, TG could reduce developing follicles and corpus luteum, and increase atretic follicles, which might be induced by the increasing levels of follicle apoptosis. The proliferation index of uterus, evaluated by histomorphological changes and the expression of Ki-67, was significantly suppressed in TG treated animals. These data suggested that TG was feasible to induce a mice model via subcutaneous injection which could mimic the manifestations of POI.
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