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>Schematic diagram of the potential mechanisms through which DHEA protects H<sub>2</sub>O<sub>2</sub>-treated BRL-3A cells from oxidative damage and apoptosis. There are at least three parallel regulation mechanisms that contribute to the protective effects of DHEA on H<sub>2</sub>O<sub>2</sub>-treated BRL-3A cells: (1) increasing cellular antioxidative enzyme activities, thus decreasing the levels of intracellular reactive oxygen species and reducing oxidative damage; (2) reducing caspase-3 protein levels through the activation of PI3K/Akt signaling pathways, rather than MAPK signaling pathways; and (3) activating specific receptors rather than androgen and estrogen receptors.</div>

Oxidative Medicine and Cellular Longevity

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Figure 8

Figure 8: 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 8 | Dehydroepiandrosterone Prevents H2O2-Induced BRL-3A Cell Oxidative Damage through Activation of PI3K/Akt Pathways rather than MAPK Pathways 