Vitisin A inhibits liver fibrosis by promoting Nrf2/HO-1 pathway and inhibiting Cuproptosis

  • Sci Rep. 2025 Dec 19;15(1):44186. doi: 10.1038/s41598-025-27836-7.
Siwen Ding  1 ,  Dishuang Hu  1 ,  Yijiu Pan  1 ,  Jiahao Wang  2 ,  Liankui Wang  3
Affiliations
  • 1. Department of Gastroenterology, Ningbo Hangzhou Bay Hospital, NingBo, 315000, Zhejiang, China.
  • 2. Department of General Surgery, the Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, Anhui, China.
  • 3. Department of Gastroenterology, Ningbo Hangzhou Bay Hospital, NingBo, 315000, Zhejiang, China. [email protected].
PMID: 41419501 DOI: 10.1038/s41598-025-27836-7
Abstract

Liver fibrosis is a characteristic pathological feature of various chronic liver diseases, which is almost irreversible and intractable. Although many natural components have been shown to have therapeutic effects on liver fibrosis, no studies have examined the effects of Vitisin A on liver fibrosis and the molecular mechanisms involved. In our study, we demonstrated that Vitisin A inhibits liver fibrosis in a concentration- dependent and time-dependent manner. We found that Vitisin A inhibits the Nrf2/HO-1 pathway while inhibiting Cuproptosis. We activated Cuproptosis and inhibited Nrf2 expression separately, and found the inhibition of hepatic fibrosis by Vitisin A was blocked. The inhibitory effect of Vitisin A on mice model of liver fibrosis was also observed. Interestingly, Vitisin A significantly restored cell viability in liver injury cell model. In conclusion, this study suggests that Vitisin A is a promising therapeutic drug for the treatment of liver fibrosis.

Keywords
Cuproptosis; LX-2; Liver fibrosis; Nrf2/HO-1 pathway; Vitisin a.
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