Work

Protective effects of taurochenodeoxycholic acid on aflatoxin B1-induced hepatic pyroptosis and gut-liver dysfunction

Year: 2025

Type: article

Abstract: Aflatoxin B1 (AFB1) is a potent mycotoxin that poses significant risks to food safety, public health, and livestock production. Taurochenodeoxycholic acid (TCDCA), a bioactive bile acid, exhibits hepatoprotective and intestinal barrier-modulating potential; however, its role in mitigating AFB1 toxicity remains unclear. This study employed a broiler model to evaluate the protective effects of TCDCA against AFB1-induced hepatic and intestinal injury. The results demonstrated that TCDCA treatment significantly improved growth performance impaired by AFB1 exposure. TCDCA alleviated hepatic lesions, decreased serum hepatic enzyme activities, and suppressed hepatocyte apoptosis and oxidative stress. Mechanistically, TCDCA modulated AFB1 detoxification by downregulating hepatic cytochrome P450 enzymes (CYP1A2 and CYP3A4), thereby reducing the formation of AFB1-DNA adducts. Furthermore, TCDCA attenuated pyroptosis and inflammation by lowering serum inflammatory cytokine contents and inhibiting activation of the hepatic NLRP3/Caspase-1/GSDMD signaling pathway. In the intestine, TCDCA improved the villus morphology, upregulated the expression of tight junction proteins including zonula occludens-1 (ZO-1), claudin-1 (CLDN1), occludin (Occludin), and mucin-2 (MUC2), reduced serum diamine oxidase (DAO) activity and D-lactate level, and restored secretory immunoglobulin A (sIgA) content, thereby strengthening intestinal barrier integrity. Additionally, 16S rRNA sequencing revealed that TCDCA mitigated AFB1-induced gut microbiota dysbiosis by increasing the abundance of Akkermansia and decreasing harmful genera such as Megamonas. Collectively, TCDCA mitigates AFB1-induced growth suppression and hepatotoxicity through mechanisms involving metabolic regulation, antioxidation, inhibition of pyroptosis and inflammation, reinforcement of intestinal barrier function, and modulation of gut microbiota.

Source: Ecotoxicology and Environmental Safety

DOI: 10.1016/j.ecoenv.2025.119432