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However, its mechanism against AFB1\u2010induced liver injury remains unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This study investigates whether NMN supplementation reduces AFB1\u2010induced liver injury through the modulation of the gut\u2010liver axis and elucidates the underlying molecular mechanism.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Mice were exposed to AFB1 (0.75\u2009mg\u00b7kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      , p.o.) for 2\u2009weeks to induce liver injury, with or without NMN (300\u2009mg\u00b7kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      , p.o.). Changes in gut microbiota were assessed via 16S rRNA sequencing, while bile acids (BAs) profiles were quantified using targeted metabolomics. The farnesoid X receptor (FXR\n                      <jats:italic>\/<\/jats:italic>\n                      NR1H4) pathway was analysed using qPCR, western blot and immunofluorescence. To establish causality, antibiotic depletion, faecal microbiota transplantation (FMT) and intestine\u2010specific FXR knockout (\n                      <jats:italic>FXR<\/jats:italic>\n                      <jats:sup>\n                        \u0394\n                        <jats:italic>IE<\/jats:italic>\n                      <\/jats:sup>\n                      ) mice were utilized.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      NMN supplementation attenuated AFB1\u2010induced liver injury, inflammation and oxidative stress, while restoring intestinal barrier integrity and reducing hepatic bile acids accumulation. Mechanistically, NMN reshaped the gut microbiota, increased bile salt hydrolase (BSH) activity and lowered intestinal conjugated bile acids, which correlated with activation of intestinal FXR\/fibroblast growth factor 15 (FGF\u201015) signalling and suppression of hepatic Cyp7a1 expression. Importantly, antibiotic depletion of gut microbiota abolished NMN protection, whereas FMT from NMN\u2010treated donors conferred resistance. Importantly, NMN failed to protect\n                      <jats:italic>FXR<\/jats:italic>\n                      <jats:sup>\n                        \u0394\n                        <jats:italic>IE<\/jats:italic>\n                      <\/jats:sup>\n                      mice, demonstrating that intestinal FXR is essential.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>NMN alleviates AFB1\u2010induced liver injury via a gut microbiota\u2010bile acid\u2010FXR axis, highlighting a novel mechanism for its hepatoprotective effects.<\/jats:p>\n                  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