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Oxidative stress then accelerates the aggregation of -synuclein which subsequently binds and sequesters available GSH, creating a destructive feedback loop of protein misfolding and antioxidant loss (Hoepken et al., 2007)

For the control group, after the same initial treatment, the FOXO4-DRI was replaced with an equal volume of PBS

This contrasts with synthetic drugs that may accumulate or produce active metabolites

Additionally, ROS activates stress-sensitive kinases (JNK, p38 MAPK) that phosphorylate IRS-2, accelerating its proteasomal degradation and further impairing -cell survival (Liu et al., 2020)

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