Effect of lycopene on TiO2 nanoforms induced oxidative stress and neuroinflammation in SH-SY5Y cells: an in vitro study.

Abstract

Due to its antioxidant action, the carotenoid lycopene has been demonstrated to have a protective effect in several disease models; however, its effect on the nanoform of titanium oxide (nano-TiO₂)-induced neurotoxicity has not yet been determined. The purpose of this study was to evaluate how lycopene affects neuronal damage brought on by nano-TiO₂ and the mechanisms involved. SH-SY5Y cells were treated with different concentrations of nano-TiO₂ for 48 hours, the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) test was used after that to evaluate cell viability. IC₅₀ of nano-TiO₂ was determined and the results revealed that IC₅₀ is equal 40 µM/mL, lycopene (10 µM) was applied to SH-SY5Y human neuroblastoma cells an hour before exposure to 40 µM nano-TiO₂. Reactive oxygen species, lipid peroxidation, nitric oxide, glutathione, superoxide dismutase, and catalase, tumor necrosis factor-alpha, interleukin 1 beta, nuclear factor kappa B, and apoptotic markers (Bcl2, Bax, and caspase-3), were measured to determine the anti-oxidant effect of lycopene. In SH-SY5Y neuroblastoma cells, pretreatment with 10 µM lycopene significantly reduced the toxicity brought on by exposure to nano-TiO₂, according to MTT assay findings and lactate dehydrogenase (LDH) cytotoxicity assessment. In cells exposed to nano-TiO₂, lycopene pretreatment significantly boosted the activity of antioxidative enzymes and reduced oxidative stress. Furthermore, when SH-SY5Y cells were subjected to nano-TiO₂, lycopene pretreatment stopped neuroinflammation and apoptosis. The findings of this study suggest that lycopene may be an effective neuroprotective against oxidative stress and neuroinflammation and may be used to stop neuronal death or injury in a variety of neurological illnesses.