The proposed mechanism for ginsenoside Rb1 to restrain oxidative stress injury. (IMAGE)
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Oxidative stress inactivated Akt to inhibit FoxO1 phosphorylation. Rb1 preserved oxidative stress-impaired Akt activation by activating Akt phosphorylation at Ser473 and promoted p-Akt binding to FoxO1. Subsequently, Rb1 promoted Akt-dependent FoxO1 phosphorylation and increased FoxO1 nuclear exclusion. Finally, the lipid peroxide production was decreased, followed by a reduction in the apoptosis factor.
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