Vitamin U Attenuates Acute Aflatoxin B1-Induced Liver Injury in Mice: Biochemical, Histological and Transcriptomic Evidence
Liyu Yang, Jiaxin Liu, Xuanxuan Zhang, Yake Wang, Shufan Liu, Chenxi Ling, Xinfeng Li, Kun Liu, Yong Huo, Guangwei Zhao, Qiuliang Xu, Hongyu Deng, Congcong LiAflatoxin B1 (AFB1) causes acute liver injury in livestock. This study evaluated whether Vitamin U could alleviate AFB1-induced hepatotoxicity in mice. AFB1 (3 mg/kg) reduced PLT, PCT, and EOS counts, caused hepatic vascular congestion, and decreased GSH-Px activity. Vitamin U (50 mg/kg) significantly improved these hematological parameters, alleviated central venous and sinusoidal congestion, increased T-SOD activity and upregulated IL-10 mRNA expression. However, Vitamin U did not significantly reverse AFB1-induced elevation of ALP or reduction in GSH-Px, nor did it affect ALT, AST, or protein levels of the Nrf2/Keap1 pathway. Transcriptomic analysis revealed enrichment of DEGs in immune- and cell cycle-related pathways, with no direct enrichment observed in the Nrf2/Keap1 pathway. Vitamin U upregulated Keap1 mRNA expression but did not alter KEAP1 protein levels. In conclusion, Vitamin U partially protects against AFB1-induced acute liver injury by ameliorating thrombocytopenia, vascular congestion, enhancing T-SOD activity, and upregulating IL-10 expression, providing preliminary experimental evidence for further investigation.