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. 2020 Jul 29;17(14):2095–2103. doi: 10.7150/ijms.45842

Figure 5.

Figure 5

Treatment of tBHQ inhibits HepG2 apoptosis and reduced oxidative stress by Nrf2/HO-1 pathway. (A) The apoptosis of HeG2 cells was measured by flow cytometry and apoptosis rates was statistical recorded (B) of each group. (C, G and H) Expression of Nrf2 and HO-1 was evaluated with or without tBHQ and CCL4 treatment. levels of MDA in HepG2 cells were analyzed in each group (D). (E, I and J) Nrf2 was knock down with siRNA-Nrf2 (siNrf2), Nrf2 and HO-1 levels reduced compared to siRNA-control (siCon) with existence of CCL4 and tBHQ in HepG2 cells. (F) Knock down Nrf2 increased MDA level in HepG2 cells treated with CCL4 and tBHQ. All experiments were performed three times independently. Data were expressed as mean ± SEM. *p < 0.05 vs. control; #p < 0.05 vs. the CCL4 group; &p < 0.05 vs. the siCon group.