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. 2022 May 7;28(17):1798–1813. doi: 10.3748/wjg.v28.i17.1798

Figure 6.

Figure 6

The activation of Sirtuin1 induced the deacetylation and inactivation of hypoxia inducible factor-1α, and subsequently rescued the progressive aggravation of acute liver failure induced by hypoxia. A: Mice were pretreated with resveratrol or exposed to hypoxia and then stimulated with lipopolysaccharide (LPS). The representative images of hematoxylin and eosin staining of liver in each group; B: The liver histological score of liver in each group; C: The levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) of mice in each group; D: Western blotting was performed to measure the levels of Sirtuin1 (Sirt1), hypoxia inducible factor (HIF)-1α, peroxisome proliferator-activated receptor alpha (PPARα) and p-AMP-activated protein kinase (AMPK) in liver tissues and the protein expression were quantified; E: The representative images of immunofluorescence staining for Acetyl-lysine and HIF-1α. Data shown are means ± standard deviations (SDs) of three separate experiments. aP < 0.05 vs Control group; bP < 0.05 vs LPS-treated group; cP < 0.05 vs LPS + Hypoxia-treated group; one-way analysis of variance combined with Bonferroni's post hoc test; the error bars indicate the SDs.