生物
毒性
对乙酰氨基酚
肠道菌群
微生物学
药品
药理学
免疫学
化学
有机化学
标识
DOI:10.1016/j.chom.2023.04.013
摘要
In this issue of Cell Host & Microbe, Zeng et al. show that a specific gut microbe causes diet-dependent attenuation of acetaminophen toxicity in mice. This link between gut microbes and toxicity is mechanistically detailed, yet intriguingly indirect, mediated by the transformation of ingested phytochemicals as opposed to the drug itself. In this issue of Cell Host & Microbe, Zeng et al. show that a specific gut microbe causes diet-dependent attenuation of acetaminophen toxicity in mice. This link between gut microbes and toxicity is mechanistically detailed, yet intriguingly indirect, mediated by the transformation of ingested phytochemicals as opposed to the drug itself. Liberation of daidzein by gut microbial β-galactosidase suppresses acetaminophen-induced hepatotoxicity in miceZeng et al.Cell Host & MicrobeApril 25, 2023In BriefGut bacterial enzymes and metabolites are linked to liver function, but the precise mechanisms are unclear. Zeng et al. reveal that Lactobacillus vaginalis exerts hepatoprotective effects during acetaminophen toxicity by liberating daidzein from the diet via β-galactosidase. These findings suggest promising therapeutic approaches and interventions. Full-Text PDF Open Access
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