Chen Jianzhao, Wang Nannan, Peng Zilun, Pang Xiufei, Ning Na, Du Qingyun, Guo Qiuping, Huang Qiuling
Center for Drug Non-Clinical Evaluation and Research, Guangzhou General Pharmaceutical Research Institute Company Limited, Guangzhou, Guangdong, 510240, People's Republic of China.
Guangzhou Baiyunshan Zhongyi Pharmaceutical Company Limited, Guangzhou, Guangdong, 510530, People's Republic of China.
J Ovarian Res. 2025 Mar 24;18(1):61. doi: 10.1186/s13048-025-01643-0.
Zishen Yutai Pill (ZYP) is a widely used Chinese patent medicine in the clinical treatment of diminished ovarian reserve (DOR) induced infertility in China. However, the pharmacological actions and underlying mechanisms of ZYP in treating DOR remain poorly understood. This study aimed to evaluate the therapeutic effects of ZYP on DOR and elucidate its potential mechanisms. Two models including tripterygium glycosides (TGs)-induced DOR rat model and pZP3-induced DOR mouse model were selected to assess the effectiveness of ZYP in treating DOR. The intervention lasted for 4 weeks in both models. ZYP administration significantly increased the primordial follicles and the serum levels of AMH both in DOR rat and mouse model. Further, ZYP regulated the apoptosis pathway and apoptosis-related molecules including PI3K-Akt signaling pathway, Bcl6 and Abtb2 in ovary of DOR rat. The ovarian apoptosis level was significantly downregulated in a dose-depended manner in ZYP groups. Thus, we demonstrate that ZYP improved the ovarian reserve in DOR models. The mechanisms of ZYP on DOR may be mediated through decreasing the apoptosis level by the regulation of PI3K-Akt signaling pathway and apoptosis molecules (Bcl6, Abtb2) in ovary.
滋肾育胎丸（ZYP）是中国临床上广泛用于治疗卵巢储备功能下降（DOR）所致不孕症的中成药。然而，ZYP治疗DOR的药理作用及潜在机制仍知之甚少。本研究旨在评估ZYP对DOR的治疗效果并阐明其潜在机制。选用雷公藤多苷（TGs）诱导的DOR大鼠模型和pZP3诱导的DOR小鼠模型来评估ZYP治疗DOR的有效性。两个模型的干预均持续4周。在DOR大鼠和小鼠模型中，给予ZYP均显著增加了原始卵泡数量和血清抗苗勒管激素（AMH）水平。此外，ZYP调节了DOR大鼠卵巢中的凋亡途径及凋亡相关分子，包括PI3K-Akt信号通路、Bcl6和Abtb2。ZYP组的卵巢凋亡水平以剂量依赖方式显著下调。因此，我们证明ZYP改善了DOR模型中的卵巢储备功能。ZYP治疗DOR的机制可能是通过调节卵巢中的PI3K-Akt信号通路和凋亡分子（Bcl6、Abtb2）来降低凋亡水平。
