<i>Bifidobacterium longum</i> BL-10 with Antioxidant Capacity Ameliorates Lipopolysaccharide-Induced Acute Liver Injury in Mice by the Nuclear Factor-κB Pathway

<i>Bifidobacterium longum</i> is frequently utilized and has broad prospects for preventing liver injury. The current research assessed the antioxidant capacity of <i>B. longum</i> BL-10 and probed its mechanism for ameliorating lipopolysaccharide (LPS)-induced acute liver injury (ALI). <i>B. longum</i> BL-10-encoded 15 antioxidant genes showed strong reducing power activity and scavenging activity of DPPH, hydroxyl radicals, and superoxide anions. The intragastric administration of <i>B. longum</i> BL-10 resulting in a marked reduction in liver function indicators (alanine aminotransferase, aspartate aminotransferase, total bilirubin, and total bile acid) and proinflammatory cytokines (TNF-α, IFN-γ, and IL-6) was indicative of ALI recovery. Following 16s RNA analysis, <i>B. longum</i> BL-10 significantly altered the richness of genera, as for the <i>Escherichia</i>-<i>Shigella</i>, <i>Lachnospiraceae</i>_NK4A136_group, and <i>Clostridia</i>_UCG-014, dramatically contributing to the formation of acetic acid and butyric acid. Meanwhile, their metabolites regulated the TLR4/NF-κB signaling pathways to alleviate hepatic injury symptoms. Overall, all the results demonstrated that <i>B. longum</i> BL-10 had excellent efficiency in preventing LPS-induced ALI.