ArticleFrontiers in pharmacology2026
Protective effects of
Article in Frontiers in pharmacology, 2026. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
7 authors.
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Abstract
Background: Diquat (DQ), a widely used bipyridyl herbicide, induces acute liver injury primarily through oxidative stress, and effective targeted therapies remain lacking. Methods: A DQ-induced acute liver injury model was established in C57BL/6 mice with LGG pretreatment and Nrf2 inhibitor (ML385) intervention. Liver function, histopathology, oxidative stress markers, and Nrf2/HO-1 expression were assessed. Results: DQ exposure markedly elevated ALT and AST levels, aggravated hepatic necrosis and inflammation, increased ROS and MDA levels, decreased SOD and GSH-Px activities, and suppressed Nrf2 and HO-1 expression. LGG pretreatment significantly alleviated liver injury and oxidative stress while restoring Nrf2/HO-1 expression. ML385 partially attenuated the protective effects of LGG. Conclusion: LGG mitigates DQ-induced acute liver injury by activating the Nrf2/HO-1 pathway and reducing oxidative stress, while 5-MIAA may represent a potential bioactive compound with similar hepatoprotective effects. These findings provide mechanistic support for probiotic-based strategies in toxicant-induced liver injury.
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