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  3. Cholic acid inhibits ovarian steroid hormone synthesis and follicular development through farnesoid X receptor signaling in mice

Cholic acid inhibits ovarian steroid hormone synthesis and follicular development through farnesoid X receptor signaling in mice

  • Int J Biol Macromol. 2025 Apr:301:140458. doi: 10.1016/j.ijbiomac.2025.140458.
Wenjun Zhu 1,  Xiaochan Cheng 1,  Hengyu Zhang 1,  Jiahao Li 1,  Li Li 2,  Hengxi Wei 2,  Shouquan Zhang 3
Affiliations

Affiliations

  • 1 State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, China.
  • 2 State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, China; National Engineering Research Center for Breeding Swine Industry, Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding, South China Agricultural University, Guangzhou 510642, China.
  • 3 State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science, South China Agricultural University, Guangzhou 510642, China; National Engineering Research Center for Breeding Swine Industry, Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding, South China Agricultural University, Guangzhou 510642, China. Electronic address: sqzhang@scau.edu.cn.
PMID: 39884637 DOI: 10.1016/j.ijbiomac.2025.140458
Abstract

This study investigated the effects of cholic acid (CA) on steroid hormone synthesis and follicular development in mouse ovaries and the regulatory mechanism of CA on the expression of steroidogenesis-related genes in granulosa cells. The mice were divided into control and CA groups, and serum and ovarian samples were collected after 1, 2, and 4 months of treatment, respectively. The results showed that CA treatment for 1, 2, and 4 months reduced ovarian weights, disrupted the estrous cycle, decreased the numbers of antral follicles and corpora lutea, and lowered the serum levels of progesterone and estradiol. Moreover, in the ovary, CA treatment upregulated the expression of farnesoid X receptor (FXR) and downregulated the expression of steroidogenesis-related genes, including StAR, CYP11A1, and HSD3B1. Mechanistically, FXR knockdown reversed the inhibitory effects of CA on steroidogenesis-related gene expression and Cholesterol uptake in granulosa cells. In vitro follicle culture experiments further confirmed that CA suppressed follicle development, decreased the mRNA expression of steroidogenesis-related genes, and reduced progesterone and estradiol secretion. Collectively, our results demonstrated that CA inhibited follicular development and steroid hormone synthesis through FXR signaling.

Keywords

Cholic acid; Farnesoid X receptor signaling; Follicular development; Steroid hormone synthesis.

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