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        <identifier>oai:figshare.com:article/33970315</identifier>
        <datestamp>2026-09-23T04:28:12Z</datestamp>
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          <dc:title>Data Sheet 1_Protective effects of Lactobacillus rhamnosus GG and 5-methoxyindole-3-acetic acid against diquat-induced acute liver injury involve activation of the Nrf2/HO-1 signaling pathway.pdf</dc:title>
          <dc:creator>Yu Wang (12152)</dc:creator>
          <dc:creator>Wenbin Gao (825538)</dc:creator>
          <dc:creator>Yonghong Wang (61187)</dc:creator>
          <dc:creator>Hongxuan Liu (14408982)</dc:creator>
          <dc:creator>Jiahao Wei (8682204)</dc:creator>
          <dc:creator>Xiaohong Zhang (32960)</dc:creator>
          <dc:creator>Jing Li (10611)</dc:creator>
          <dc:subject>Pharmacology</dc:subject>
          <dc:subject>5-methoxyindole-3-acetic acid</dc:subject>
          <dc:subject>acute liver injury</dc:subject>
          <dc:subject>diquat</dc:subject>
          <dc:subject>Lactobacillus rhamnosus GG</dc:subject>
          <dc:subject>Nrf2/HO-1 signaling pathway</dc:subject>
          <dc:subject>oxidative stress</dc:subject>
          <dc:description>Background&lt;p&gt;Diquat (DQ), a widely used bipyridyl herbicide, induces acute liver injury primarily through oxidative stress, and effective targeted therapies remain lacking. Lactobacillus rhamnosus GG (LGG) exhibits antioxidant potential, but its role in DQ-induced liver injury has not been fully clarified. This study investigated the protective effects of LGG and its associated metabolite 5-methoxyindole-3-acetic acid (5-MIAA) and explored the underlying mechanisms.&lt;/p&gt;Methods&lt;p&gt;A DQ-induced acute liver injury model was established in C57BL/6 mice with LGG pretreatment and Nrf2 inhibitor (ML385) intervention. Liver function, histopathology, oxidative stress markers, and Nrf2/HO-1 expression were assessed. In vitro, DQ-treated HepG2 cells were exposed to varying concentrations of 5-MIAA, and cell viability and pathway-related molecules were analyzed using CCK-8 and Western blot.&lt;/p&gt;Results&lt;p&gt;DQ exposure markedly elevated ALT and AST levels, aggravated hepatic necrosis and inflammation, increased ROS and MDA levels, decreased SOD and GSH-Px activities, and suppressed Nrf2 and HO-1 expression. LGG pretreatment significantly alleviated liver injury and oxidative stress while restoring Nrf2/HO-1 expression. ML385 partially attenuated the protective effects of LGG. In vitro, 5-MIAA dose-dependently improved viability of DQ-injured HepG2 cells and upregulated Nrf2 and HO-1 expression.&lt;/p&gt;Conclusion&lt;p&gt;LGG mitigates DQ-induced acute liver injury by activating the Nrf2/HO-1 pathway and reducing oxidative stress, while 5-MIAA may represent a potential bioactive compound with similar hepatoprotective effects. These findings provide mechanistic support for probiotic-based strategies in toxicant-induced liver injury.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-23T04:28:12Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fphar.2026.1904443.s002</dc:identifier>
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          <dc:rights>CC BY 4.0</dc:rights>
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