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. 2019 Oct 11;71(3):1037–1054. doi: 10.1002/hep.30882

Figure 8.

Figure 8

TAK1 mediated the effect of Steap3 on hepatocyte inflammation and apoptosis after H/R treatment. (A) Western blot analysis of total and phosphorylated TAK1, JNK, and p38 in Steap3 overexpressed hepatocytes treated with NG25 subjected to H/R challenge. GAPDH served as the loading control. Representative of three independent experiments. (B) mRNA levels of proinflammatory factors (Tnf‐α, Il6, Il1b, and Ccl2) in Steap3 overexpressed hepatocytes treated with NG25 subjected to H/R challenge. (C) Protein levels of NF‐κB signaling pathway molecules in Steap3 overexpressed hepatocytes treated with NG25 subjected to H/R challenge. GAPDH served as the loading control. Representative of three independent experiments. (D) mRNA levels of apoptosis‐related genes (Bad, Bax, and Bcl2) in Steap3 overexpressed hepatocytes treated with NG25 subjected to H/R challenge. (E) Western blot analysis of the Bax, Bcl2, and cleaved caspase‐3 levels in Steap3 overexpressed hepatocytes treated with NG25 subjected to H/R challenge. GAPDH served as the loading control. Representative of three independent experiments. All data are shown as the mean ± SD. Levels of statistical significance are indicated as *P < 0.05, **P < 0.01. For statistical analysis, one‐way ANOVAs with Bonferroni’s post hoc analysis or Tamhane’s T2 post hoc analysis were used. Abbreviations: IκBα, inhibitory κBα; IKKβ, IκB kinase β.