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The effect of CGA on metabolic dysfunction-associated steatohepatitis (MASH) and the potential mechanism based on bile acids (BAs) alternative biosynthesis pathway\u2014farnesoid X receptor (FXR) axis are investigated here.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Alanine aminotransferase, hepatic triglyceride, malondialdehyde (MDA), BAs, fatty acids oxidation (FAO) activity, mRNA of inflammatory cytokines, \u03b1-smooth muscle actin (\u03b1-SMA), transforming growth factor-\u03b2, collagen type I, and FAO enzymes were detected. Liver sections underwent hematoxylin\u2013eosin, Oil Red O, and Sirius red staining, and immunohistochemistry assay of F4\/80 and \u03b1-SMA. Protein expression of peroxisome proliferator-activated receptor \u03b1 (PPAR-\u03b1), FXR, BAs biosynthesis enzymes, small heterodimer partner (SHP), bile salt export pump (BSEP), adenosine triphosphate-binding cassette sub-family B member 4 (ABCB4) and nuclear factor-kappa B were detected.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key findings<\/jats:title>\n                    <jats:p>CGA ameliorated MASH, restoring FAO, PPAR-\u03b1, and FXR, accompanied by increased chenodeoxycholic acid proportion in the FXR agonist BAs pool, BAs alternative biosynthesis, and the FXR targets including SHP, BSEP, and ABCB4.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>CGA ameliorates MASH, promoting the hepatic BAs alternative biosynthesis pathway to activate FXR-PPAR\u03b1 restoring FAO.<\/jats:p>\n                  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