Dehydroepiandrosterone Prevents H<sub>2</sub>O<sub>2</sub>-Induced BRL-3A Cell Oxidative Damage through Activation of PI3K/Akt Pathways rather than MAPK Pathways

<div>Effects of DHEA on Bax and caspase-3 protein expression in H<sub>2</sub>O<sub>2</sub>-treated BRL-3A cells. (a) Immunoblot of Bax and caspase-3 in BRL-3A cells pretreated with 1-100 <i>μ</i>M DHEA (24 h) and then exposed to 150 <i>μ</i>M H<sub>2</sub>O<sub>2</sub> (2 h). (b) Bax protein expression. (c) Caspase-3 protein expression. (d) Immunoblot of Bax and caspase-3 in BRL-3A cells pretreated with 50 <i>μ</i>M of the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 or vehicle for 1 h before exposure to 0, 1, 10, or 100 <i>μ</i>M DHEA (24 h) and then 150 <i>μ</i>M H<sub>2</sub>O<sub>2</sub> (2 h). (e) Bax protein expression. (f) Caspase-3 protein expression. 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Oxidative Medicine and Cellular Longevity

fig7

Figure 7

Figure 7: Dehydroepiandrosterone Prevents H<sub>2</sub>O<sub>2</sub>-Induced BRL-3A Cell Oxidative Damage through Activation of PI3K/Akt Pathways rather than MAPK Pathways 

Figure 7 | Dehydroepiandrosterone Prevents H2O2-Induced BRL-3A Cell Oxidative Damage through Activation of PI3K/Akt Pathways rather than MAPK Pathways 