Uridine diphosphate glucuronosyltransferase 1A1 prevents the progression of liver injury

Figure 8 Interference with upregulation of uridine diphosphate glucuronosyltransferase 1A1 exacerbates hepatic endoplasmic reticulum stress, oxidative stress, and lipid metabolism disorder during liver injury. A-C: Malondialdehyde (MDA), triglyceride (TG), and total cholesterol (TC) contents in the livers of mice with carbon tetrachloride (CCl₄)-mediated liver injury; D: Related protein expressions in mice with CCl₄-mediated liver injury; E-G: MDA, TG, and TC contents in the livers of mice were measured in the Ugt1a1 knockout model after treatment with CCl₄; H: Related protein expressions in CCl₄- mediated model mice with Ugt1a1 knockout; I-K: MDA, TG, and TC contents in the livers of mice with concanavalin A (ConA)-mediated liver injury; L: Related protein expressions in mice with ConA-mediated liver injury; M-O: MDA, TG, and TC contents in the livers of mice were measured in the Ugt1a1 knockout model after treatment with CCl₄; P: Related protein expressions in ConA-mediated model mice with Ugt1a1 knockout. ^aP < 0.05, ^bP < 0.01 vs the 0 h or control group; ^dP < 0.01 vs the CCl₄ groups or ConA groups. MDA: Malondialdehyde; TG: Triglyceride; TC: Total cholesterol; UGT1A1: Uridine diphosphate glucuronosyltransferase 1A1; MTP: Microsomal triglyceride transfer protein; MCAD: Medium-chain acyl-CoA dehydrogenase; SREBP1c: Cleaved sterol regulatory element-binding protein 1; ACSL4: Acyl-CoA synthetase long chain family member 4; GRP78: 78-kDa glucose-regulated protein; UCP2: Uncoupling protein-2; CCl₄: Carbon tetrachloride; ConA: Concanavalin A; KO: Knockout; GAPDH: Glyceraldehyde 3 phosphate dehydrogenase.