Yijing Decoction improves oocyte quality and inhibits lactate accumulation in mice with diminished ovarian reserve

Diminished ovarian reserve (DOR) is characterized by a decline in both oocyte quantity and quality, leading to compromised fertility. Yijing Decoction (YJD) has demonstrated promising therapeutic potential in DOR management. Nevertheless, the mechanisms driving this phenomenon are still largely unclear. This study is designed to comprehensively assess the effects of YJD on ovarian reserve function and oocyte quality in DOR mice, while investigating its potential underlying mechanisms of action.

A DOR mouse model was established by administering cyclophosphamide via a single intraperitoneal injection. The therapeutic efficacy of YJD was systematically assessed through multiple functional and histological parameters, including ovarian index, estrous cycle regularity, serum sex hormone levels (FSH, LH, E₂, AMH, and INH-B), and follicle counts, as well as the number, quality, and spindle morphology of metaphase I (MI) oocytes. To elucidate the underlying molecular mechanisms, ATP levels, pyruvate uptake, and lactate production were further quantified using commercially available ATP, pyruvate, and lactate assay kits. Additionally, immunofluorescence microscopy was employed to assess the protein expression levels of glycolysis-related proteins, including GLUT1, GLUT4, and LDHA, as well as components of the SIRT3/HIF-1α/PDK1 signaling axis in MI oocytes.

YJD treatment improved ovarian reserve function and oocyte quality in DOR mice, as evidenced by increased ovulated oocyte numbers, improved spindle integrity, and restored ATP levels. In addition, YJD treatment was associated with reduced expression of glycolysis-related proteins, including GLUT1, GLUT4, and LDHA, as well as decreased pyruvate uptake and lactate production in MI oocytes. YJD treatment also partially restored the expression pattern of the SIRT3/HIF-1α/PDK1 signaling pathway in DOR oocytes.

YJD improves oocyte quality in DOR mice, and its protective effects may be associated with the regulation of lactate metabolism and the SIRT3/HIF-1α/PDK1 signaling pathway.