Fig. 2

Excessive ROS production during liver I/R injury decreases DHX58 expression. a DHX58 protein level in primary hepatocytes treated with H₂O₂ was examined by Western blotting. b Dhx58 mRNA level in primary hepatocytes treated with H₂O₂ was examined by qRT-PCR. c DHX58 protein level in liver tissues with NAC or BHA pre-treatment and then I/R was examined by Western blotting. d Dhx58 mRNA level in liver tissues with NAC or BHA pre-treatment and then I/R was examined by qRT-PCR. e DHX58 protein level in primary hepatocytes with NAC or BHA pre-treatment and then H/R was examined by Western blotting. f Dhx58 mRNA level in primary hepatocytes with NAC or BHA pre-treatment and then H/R was examined by qRT-PCR. g DHX58 protein level in primary hepatocytes with NAC or BHA pre-treatment and then H₂O₂ (2 mmol/L) administration for 3 h was examined by Western blotting. h Dhx58 mRNA level in primary hepatocytes with NAC or BHA pre-treatment and then H₂O₂ (2 mmol/L) administration for 3 h was examined by qRT-PCR. Data are shown as mean ± SD (n = 3) or photographs from one representative of three independent experiments. ^*P < 0.05, ^**P < 0.01. ROS reactive oxygen species, I/R ischemia/reperfusion, DHX58 DExH-box helicase 58, NAC N-acetylcysteine, BHA butylated hydroxyanisole, H/R hypoxia/re-oxygenation, SD standard deviation