ArticleDrug design, development and therapy2025
Butein Alleviates Non-Alcoholic Steatohepatitis in Leptin-Deficient Mice by Modulating the PDE4/cAMP/p-CREB Pathway.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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10 authors.
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Abstract
Purpose: Non-alcoholic steatohepatitis (NASH) is a prevalent liver disease characterized by steatosis, inflammation, and liver injury. Despite its increasing incidence, effective treatments are limited. Butein, a flavonoid with anti-cancer, anti-inflammatory, and antioxidant properties, has not been thoroughly studied for its potential therapeutic effects in NASH. This study aimed to evaluate the effects of butein in NASH using both in vivo and in vitro experimental models, with emphasis on elucidating the underlying molecular signaling mechanisms. Methods: The leptin-deficient ( Results: Butein treatment resulted in significant amelioration of glucolipid metabolism dysregulation, hepatic inflammation, and liver fibrosis in the mouse model, potentially mediated through modulation of the PDE4/cAMP/p-CREB signaling pathway. In in vitro experimental models, butein effectively attenuated lipid-induced oxidative stress in HepG2 cells and reduced inflammatory and fibrotic responses in LX-2 cells, demonstrating consistent protective effects across both experimental models. Conclusion: These findings establish the protective effects of butein against NASH progression through PDE4/cAMP/p-CREB pathway modulation, supporting its potential as a therapeutic candidate for NASH treatment pending further clinical validation.
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