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. 2014 Jun 13;289(33):22672–22691. doi: 10.1074/jbc.M114.552141

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© 2014 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 5. — Hmgb1^fl/flAlb-Cre mice are protected from ALD. H&E staining from liver and kidney from non-treated Hmgb1^fl^/^flAlb-Cre and Hmgb1^fl^/^fl^−/−Alb-Cre⁻ littermates is shown (A). HMGB1 IHC from liver and kidney from non-treated Hmgb1^fl^/^flAlb-Cre mice and Hmgb1^fl^/^fl^−/−Alb-Cre⁻ mice is shown (B). The livers from Hmgb1^fl^/^flAlb-Cre mice confirmed the absence of HMGB1-positive staining in hepatocytes compared with Hmgb1^fl^/^fl^−/−Alb-Cre⁻ mice (red arrow). Hmgb1^fl^/^flAlb-Cre and Hmgb1^fl^/^fl^−/−Alb-Cre⁻ littermates were fed for 7 weeks the control or the ethanol Lieber-DeCarli diet. In IHC for HMGB1, the red arrow indicates HMGB1 positive staining in the nucleus and negative staining in the cytoplasm, and the yellow arrow points to HMGB1 negative staining in the nucleus and positive staining in the cytoplasm (C, top). Western blot analysis for HMGB1 in the ethanol-fed mice only is shown (C, bottom). Images show the gross appearance of the livers from control and ethanol-fed Hmgb1^fl^/^flAlb-Cre and Hmgb1^fl^/^fl^−/−Alb-Cre⁻ mice (D, top). H&E staining shows steatosis (black arrow) and inflammation (orange arrow) (D, middle). Serum alanine aminotransferase (ALT) activity (units/liter), serum triglycerides (TG) (mg/dl), and liver triglycerides (mg/g of protein) along with the scores for steatosis, inflammation, and necrosis classified according to the Brunt scoring system (40) are shown (D, bottom). n = 10/group. *, p < 0.05; **p < 0.01 for ethanol versus control. •, p < 0.05; ••, p < 0.01 for Hmgb1^fl^/^flAlb-Cre versus Hmgb1^fl^/^fl^−/−Alb-Cre⁻. Hmgb1 ablation increases CPT1, pAMPKα, and pPPARα expression and enhances LDL plus VLDL export, preventing steatosis and liver injury in mice. Western blot analysis revealed an increase in the expression of CPT1, pAMPKα, and pPPARα in ethanol-fed Hmgb1^fl^/^flAlb-Cre mice compared with Hmgb1^fl^/^fl^−/−Alb-Cre⁻ littermates (E). Serum and liver LDL plus VLDL levels in control and ethanol-fed Hmgb1^fl^/^flAlb-Cre and Hmgb1^fl^/^fl^−/−Alb-Cre⁻ mice are shown (F). Results are expressed as average values ± S.E. n = 10/group. *, p < 0.05; **, p < 0.01 for ethanol versus control. •, p < 0.05; •••, p < 0.001 for Hmgb1^fl^/^flAlb-Cre versus Hmgb1^fl^/^fl^−/−Alb-Cre⁻. PV, portal vein; CV, central vein.

FIGURE 5. — Hmgb1^fl/flAlb-Cre mice are protected from ALD. H&E staining from liver and kidney from non-treated Hmgb1^fl^/^flAlb-Cre and Hmgb1^fl^/^fl^−/−Alb-Cre⁻ littermates is shown (A). HMGB1 IHC from liver and kidney from non-treated Hmgb1^fl^/^flAlb-Cre mice and Hmgb1^fl^/^fl^−/−Alb-Cre⁻ mice is shown (B). The livers from Hmgb1^fl^/^flAlb-Cre mice confirmed the absence of HMGB1-positive staining in hepatocytes compared with Hmgb1^fl^/^fl^−/−Alb-Cre⁻ mice (red arrow). Hmgb1^fl^/^flAlb-Cre and Hmgb1^fl^/^fl^−/−Alb-Cre⁻ littermates were fed for 7 weeks the control or the ethanol Lieber-DeCarli diet. In IHC for HMGB1, the red arrow indicates HMGB1 positive staining in the nucleus and negative staining in the cytoplasm, and the yellow arrow points to HMGB1 negative staining in the nucleus and positive staining in the cytoplasm (C, top). Western blot analysis for HMGB1 in the ethanol-fed mice only is shown (C, bottom). Images show the gross appearance of the livers from control and ethanol-fed Hmgb1^fl^/^flAlb-Cre and Hmgb1^fl^/^fl^−/−Alb-Cre⁻ mice (D, top). H&E staining shows steatosis (black arrow) and inflammation (orange arrow) (D, middle). Serum alanine aminotransferase (ALT) activity (units/liter), serum triglycerides (TG) (mg/dl), and liver triglycerides (mg/g of protein) along with the scores for steatosis, inflammation, and necrosis classified according to the Brunt scoring system (40) are shown (D, bottom). n = 10/group. *, p < 0.05; **p < 0.01 for ethanol versus control. •, p < 0.05; ••, p < 0.01 for Hmgb1^fl^/^flAlb-Cre versus Hmgb1^fl^/^fl^−/−Alb-Cre⁻. Hmgb1 ablation increases CPT1, pAMPKα, and pPPARα expression and enhances LDL plus VLDL export, preventing steatosis and liver injury in mice. Western blot analysis revealed an increase in the expression of CPT1, pAMPKα, and pPPARα in ethanol-fed Hmgb1^fl^/^flAlb-Cre mice compared with Hmgb1^fl^/^fl^−/−Alb-Cre⁻ littermates (E). Serum and liver LDL plus VLDL levels in control and ethanol-fed Hmgb1^fl^/^flAlb-Cre and Hmgb1^fl^/^fl^−/−Alb-Cre⁻ mice are shown (F). Results are expressed as average values ± S.E. n = 10/group. *, p < 0.05; **, p < 0.01 for ethanol versus control. •, p < 0.05; •••, p < 0.001 for Hmgb1^fl^/^flAlb-Cre versus Hmgb1^fl^/^fl^−/−Alb-Cre⁻. PV, portal vein; CV, central vein.