ArticleJournal of physiology and biochemistry2023
Antifibrogenic and apoptotic effects of Ocoxin in cultured rat hepatic stellate cells.
Article in Journal of physiology and biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Contribution of p38 MAPK in liver fibrosis: An overview of mechanisms, signaling pathways, and therapeutic targets (Review).International journal of molecular medicine · 2026Review
- Natural drugs modulate MAPK: targets and strategies for liver fibrosis treatment.Frontiers in pharmacology · 2026Review
- Liraglutide inhibits the proliferation of rat hepatic stellate cells under high glucose conditions by suppressing the ERK signaling pathway.Scientific reports · 2025Article
- Exploring the alleviating effects ofFrontiers in microbiology · 2024Article
- Frontiers in fatty liver: recent advances in pathogenic mechanisms, assessment of patients' prognosis and pharmacotherapy : MASLD: new pathogenic mechanisms, risk assessment tools and drug therapies.Journal of physiology and biochemistry · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
Ocoxin is a nutritional supplement that has been shown to exert antioxidant and immunomodulatory responses in patients with chronic hepatitis C. The present work aimed to determine the effects of Ocoxin on activated hepatic stellate cells (HSC), the cell type mainly responsible for collagen deposition in the fibrotic liver. Ocoxin was found to reduce the survival of a cell line of immortalized non-tumoral rat HSC in a dose-response fashion and to diminish collagen type I levels. This latter effect was observed even at doses not affecting cell survival, pointing to an antifibrogenic action for the supplement. The decrease in viability exerted by Ocoxin on HSC correlated with an increase in histone-associated fragments in the cytoplasm and with increased activity of caspase-3, indicating the induction of apoptosis. To determine the molecular mechanisms mediating Ocoxin-induced apoptosis, the activation of members of the MAPK family was analyzed. Incubation of HSC with Ocoxin caused a transient and dramatic enhancement on ERK, JNK, and p38 MAPK phosphorylation levels. Using specific inhibitors for these enzymes, p38 MAPK was identified as a key mediator of the apoptotic effect of Ocoxin on HSC.
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