Rutin from Ruta Chalapensis Mitigates Rotenone-Induced Mitochondrial Dysfunction, Oxidative Stress, and Apoptosis

neurons against oxidative stress, mitochondrial malfunction, and cell death caused by rotenone. According to the MTT
viability test, SH-SY5Y cells were assigned to four different experimental groups. The groups comprised rotenone (100
nM), a control, rutin (10 μM) alone, and rutin (10 μM) in combination with rotenone (100 nM). Rotenone caused
mitochondrial malfunction, oxidative stress, and cytotoxicity in SH-SY5Y cells. Rutin, however, markedly reduced the
intensity of these effects. The protective effect of rutin against rotenone was evident from its ability to boost Bcl-2
expression and inhibit Bax and caspase-3 activation. Rutin was found to protect cells by modulating the production of p-
AKT, p-GSK-3 beta, and p-PI3K. Through regulation of PI3K/Akt/GSK-3β signaling, rutin suppressed oxidative toxicity,
preserved mitochondrial integrity, and limited rotenone-induced apoptosis. Additional research in rats is required to fully
determine rutin’s effectiveness as a prospective Parkinson’s disease therapy.