Fig. 5

Knockdown of H19 up-regulates PI3K–Akt–mTOR pathway in the Hep G2 cells. H19 siRNA was used as the knockdown of H19, 5 mM 3-MA in 24 h reoxygenation was used to inhibit autophagy and 50 nM Rapa (rapamycin) in 24 h reoxygenation was used to inhibit mTOR and activate autophagy. a Knockdown of H19 increases the phosphorylation of PI3K, Akt and mTOR was detected using western blot analysis. The graphs represent the optical density of the bands of phospho-PI3K (p-PI3K), Akt (p-Akt) and mTOR (p-mTOR) normalized with the expression of total-PI3K (t-PI3K), Akt (t-Akt) and mTOR (t-mTOR). The phosphorylated levels in the control group were considered the basal levels, and the others are expressed as fold change from the control group. All data were from four independent experiments. **p < 0.01 vs. control group; ^##p < 0.01 vs. 8 h/24R group. b Knockdown of H19 cancelled the effect of Rapa on the phosphorylation of PI3K, Akt and mTOR. The graphs represent the optical density of the bands of phospho-PI3K (p-PI3K), Akt (p-Akt) and mTOR (p-mTOR) normalized with the expression of total-PI3K (t-PI3K), Akt (t-Akt) and mTOR (t-mTOR). The phosphorylated levels in the control group were considered the basal levels, and the others are expressed as fold change from the control group. All data were from four independent experiments. **p < 0.01 vs. control group; ^##p < 0.01 vs. 8 h/24R group; ^$$p < 0.01 vs. 8 h/24R + Rapa group