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The molecular mechanism of GP treatment mediating oxidative stress in mice with depression-like behavior via the Six3os1/Fezf1/AKT. In CUMS-induced mice, miR-511-3p targets and inhibits Fezf1, thus stimulating oxidative stress of neurons. After GP treatment, Six3os1 expression is upregulated, which increases Fezf1 expression by binding to miR-511-3p and then activates AKT signaling pathway, thus alleviating oxidative stress in mice with depression-like behavior.
