数字农科院2.0

Lactobacillus reuteri alleviates diquat induced hepatic impairment and mitochondrial dysfunction via activation of the Nrf2 antioxidant system and suppression of NF-κB inflammatory response

文献类型： 外文期刊

作者： Shenao Zhan;Lianchi Wu;Yujie Lv;Weichen Huang;Chaoyue Ge;Zhaoying Hu;Xinyu Shen;Gang Lin;Dongyou Yu;Bing Liu

作者机构：

关键词： Apoptosis;Inflammation;Liver injury;Mitochondrial dysfunction;Oxidative stress

期刊名称： Poultry Science

ISSN： 0032-5791

年卷期： 2025 年 104 卷 5 期

页码：

收录情况： SCIE（2025版）

摘要： Accumulating evidence has shown that elevated oxidative stress and inflammatory response leads to hepatic impairment and dysfunction of hens during the aging process. This study was conducted to investigate the potential regulatory mechanisms of Lactobacillus reuteri (L. reuteri) in alleviating hepatic oxidative stress and dysfunction induced by diquat (DQ) exposure. A total of 480 48-wk-old Jingbai hens were randomly assigned to 4 groups: control group (Con), L. reuteri group (L.R), diquat-challenged group (DQ), and L. reuteri protective group (L.R+DQ). The results demonstrated that DQ exposure induced oxidative damages and lipid metabolism disorders manifested as the elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, triglyceride (TC) contents in serum and lipid accumulation in liver. L. reuteri supplementation alleviated DQ-induced liver oxidative injury, reflected by repairing the morphology of liver and decreasing the AST and ALT activities in serum. L. reuteri decreased the hepatic malonaldehyde (MDA) accumulation and enhanced the total antioxidant capacity (T-AOC), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities in liver through regulating the nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) mediated antioxidant system. In addition, L. reuteri curtailed reactive oxygen species (ROS) production and mitigated the depletion of membrane potential and thus recovering mitochondrial function disturbed by DQ challenge. Moreover, L. reuteri inhibited hepatic toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB) pathway activation, downregulated the pro-inflammatory-response-related gene expressions (IL-1β, TNF-α, and IL-6) and the phosphorylation levels of IκBα, and p65 in liver and thus reducing hepatic inflammatory response and apoptosis. Overall, the findings indicate that L. reuteri provides significant protection against oxidative stress, mitochondrial impairment, inflammatory response and apoptosis caused by DQ in laying hens, and highlight its potential as a therapeutic probiotic for alleviating oxidative stress and mitochondrial dysfunction to prolong the health of aging poultry.

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