International Journal of Drug Delivery Technology
Volume 15, Issue 4

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

Jayanthi P1, Shobana C2*. 

1Department of Biochemistry, School of Life Sciences, Vels Institute of Science, Technology and Advanced Studies, Chennai, Tamil Nadu, India.

2*Associate Professor, Department of Biochemistry, School of Life Sciences, Vels Institute of Science, Technology and Advanced Studies, Chennai, Tamil Nadu, India.

Received: 14th Aug, 2025; Revised: 19th Sep 2025; Accepted: 20th Nov, 2025; Available Online: 30th Nov, 2025 

ABSTRACT

This study intends to employ an in vitro model to investigate whether rutin, a plant-derived flavanol glycoside, may protect 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.

Keywords: Rutin, Ruta chalepensis, Rotenone, Mitochondrial dysfunction, Oxidative stress, PI3K/Akt/GSK-3β pathway.

How to cite this article: Jayanthi P, Shobana C. Rutin from Ruta chalapensis mitigates rotenone-induced mitochondrial dysfunction, oxidative stress, and apoptosis.. Int J Drug Deliv Technol. 2025;15(4): 1506-1513, DOI: 10.25258/ijddt.15.4.7