Acute liver failure (ALF) is a life-threatening clinical condition resulting from massive apoptosis of hepatocytes. This study aims to examine the protective effects of Lactobacillus plantarum C88 on LPS/D-GalN-induced ALF and elucidate its underlying molecular mechanisms in mice. The results showed that L. plantarum C88 pretreatment significantly reduced the levels of plasma ALT and AST in mice with LPS/D-GalN–induced liver injury. L. plantarum C88 pretreatment decreased the secretion of inflammatory cytokines. In addition, L. plantarum C88 remarkably increased the expression levels and nuclear translocations of Nrf2 mRNA in liver tissues, but inhibited NF-κB nuclear translocations and P65, P38 phosphorylation levels. Moreover, L. plantarum C88 enhanced the intestinal mucosal barrier by upregulating the expressions of tight junction proteins as well as HIF-1α. These results suggest that L. plantarum C88 protects against ALF associated with Nrf2 and the MAPK/NF-κB signaling pathways.

急性肝衰竭（ALF）是由肝细胞大量凋亡导致的危及生命的临床疾病。这项研究旨在检查植物乳杆菌C88对LPS / D-GalN诱导的ALF的保护作用，并阐明其在小鼠中的潜在分子机制。结果表明，植物乳杆菌C88预处理可显着降低LPS / D-GalN诱导的肝损伤小鼠的血浆ALT和AST水平。植物乳杆菌C88预处理减少了炎性细胞因子的分泌。此外，植物乳杆菌C88显着提高了肝组织中Nrf2 mRNA的表达水平和核易位，但抑制了NF-κB核易位以及P65，P38磷酸化水平。而且，植物乳杆菌C88通过上调紧密连接蛋白以及HIF-1α的表达来增强肠粘膜屏障。这些结果表明，植物乳杆菌C88可以防止与Nrf2和MAPK /NF-κB信号通路相关的ALF。