Open Access

Baicalin mitigates polycystic ovary syndrome‑associated non‑alcoholic fatty liver disease by inhibiting the AR/SREBP1 axis

  • Authors:
    • Bi-Hui Jin
    • Han Xu
    • Zi-Yan Zhang
    • Yu-Hang Fan
    • Chun-Yan Jiang
    • Shao-Long Qi
    • Chen-Yu Xiao
    • Xiao-Hua Fu
    • Ling-Bo Qian
  • View Affiliations

  • Published online on: September 8, 2025     https://doi.org/10.3892/ijmm.2025.5630
  • Article Number: 189
  • Copyright: © Jin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Polycystic ovary syndrome (PCOS) is a common endocrine disorder frequently associated with metabolic disturbances, such as non‑alcoholic fatty liver disease (NAFLD), driven by hyperandrogenism‑induced lipogenesis. Baicalin (BA), a flavonoid derived from Scutellaria baicalensis, exhibits therapeutic potential in the treatment of PCOS; however, the specific mechanisms against PCOS‑associated NAFLD remain unclear. In the present study, a PCOS mouse model was established via subcutaneous implantation of dihydrotestosterone. Model validation confirmed irregular estrous cycles, ovarian histopathological abnormalities and altered serum hormone levels. Treatment with BA markedly alleviated NAFLD‑associated metabolic abnormalities, including central obesity, dyslipidemia and hepatic steatosis. Moreover, liver transcriptomics indicated that BA modulated lipid metabolism primarily through sterol regulatory element‑binding protein 1 (SREBP1)‑mediated lipogenesis. Results of western blot analysis confirmed that BA suppressed hepatic protein expression of SREBP1 and its downstream lipogenic enzymes, fatty acid synthase and acetyl‑CoA carboxylase, indicating inhibition of hepatic lipogenesis. As androgen receptor (AR) functions as an upstream transcriptional regulator of SREBP1, network pharmacological analysis highlighted AR as a potential target of BA. Molecular docking predicted the BA‑AR binding site, guiding purification of truncated AR protein for isothermal titration calorimetry (ITC). Subsequently ITC was used to confirm the specific BA‑AR binding affinity. Luciferase reporter assays in MDA‑kb2 cells demonstrated that BA inhibited AR transcriptional activity. Collectively, the results of the present study indicated that BA ameliorates PCOS‑associated NAFLD through targeting the AR/SREBP1 axis, highlighting its potential as a therapeutic strategy for managing lipid metabolism disorders in PCOS.
View Figures
View References

Related Articles

Journal Cover

November-2025
Volume 56 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Jin B, Xu H, Zhang Z, Fan Y, Jiang C, Qi S, Xiao C, Fu X and Qian L: Baicalin mitigates polycystic ovary syndrome‑associated non‑alcoholic fatty liver disease by inhibiting the AR/SREBP1 axis. Int J Mol Med 56: 189, 2025.
APA
Jin, B., Xu, H., Zhang, Z., Fan, Y., Jiang, C., Qi, S. ... Qian, L. (2025). Baicalin mitigates polycystic ovary syndrome‑associated non‑alcoholic fatty liver disease by inhibiting the AR/SREBP1 axis. International Journal of Molecular Medicine, 56, 189. https://doi.org/10.3892/ijmm.2025.5630
MLA
Jin, B., Xu, H., Zhang, Z., Fan, Y., Jiang, C., Qi, S., Xiao, C., Fu, X., Qian, L."Baicalin mitigates polycystic ovary syndrome‑associated non‑alcoholic fatty liver disease by inhibiting the AR/SREBP1 axis". International Journal of Molecular Medicine 56.5 (2025): 189.
Chicago
Jin, B., Xu, H., Zhang, Z., Fan, Y., Jiang, C., Qi, S., Xiao, C., Fu, X., Qian, L."Baicalin mitigates polycystic ovary syndrome‑associated non‑alcoholic fatty liver disease by inhibiting the AR/SREBP1 axis". International Journal of Molecular Medicine 56, no. 5 (2025): 189. https://doi.org/10.3892/ijmm.2025.5630