NEUROPROTECTIVE EFFECT OF 7,3´-DIHYDROXYFLAVONE AGAINST PACLITAXEL-INDUCED NEUROTOXICITY IN SH-SY5Y NEUROBLASTOMA CELL LINE: AN IN VITRO MODEL

Objectives: Paclitaxel (PT) induced peripheral neuropathy is associated with the neurotoxic effects of this chemotherapeutic drug. As a result, the need for natural substances that can mitigate neural toxicity is rising. This study investigated the Neuroprotective effects of 7,3´-dihydroxyflavone (7,3´-DHF) on PT-induced neurotoxicity in SH-SY5Y neuroblastoma cells. Methods: The cells were exposed to a 1 μM concentration of PT, and the protective effects of various concentrations of 7,3´-DHF were evaluated. The reactive oxygen species (ROS) level in SH-SY5Y cells was measured using confocal fluorescence microscopy. The concentration of proinflammatory cytokines, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) was determined by enzyme-linked immunosorbent assay. Results: Treatment of SH-SY5Y cells with 1 μM PT significantly reduced cell viability to 19±4.8%. However, treatment with 7,3´-DHF in PT-exposed cells elevated SH-SY5Y cell viability in a dose-dependent manner, with viability reaching 55.34±3.8% and 83.93±4.1% at 7,3´-DHF concentrations of 75 μg/mL and 100 μg/mL, respectively. PT exposure elevated ROS levels in SH-SY5Y cells, but the presence of 7,3´-DHF reduced ROS levels against PT-induced toxicity. In addition, treatment with 7,3´-DHF lowered the increased levels of IL-6 and TNF-α induced by PT exposure. Conclusion: 7,3´-DHF effectively preserved the viability of SH-SY5Y cells under PT-induced toxicity. This protective effect was mediated through the suppression of ROS production and the attenuation of proinflammatory cytokine release, highlighting its potential as a neuroprotective agent.