Almeer Rafa, Alyami Nouf M
Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia.
Drug Chem Toxicol. 2025 Jan;48(1):51-61. doi: 10.1080/01480545.2024.2397429. Epub 2024 Sep 3.
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-TiO)-induced neurotoxicity has not yet been determined. The purpose of this study was to evaluate how lycopene affects neuronal damage brought on by nano-TiO and the mechanisms involved. SH-SY5Y cells were treated with different concentrations of nano-TiO for 48 hours, the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) test was used after that to evaluate cell viability. IC of nano-TiO was determined and the results revealed that IC is equal 40 µM/mL, lycopene (10 µM) was applied to SH-SY5Y human neuroblastoma cells an hour before exposure to 40 µM nano-TiO. 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-TiO, according to MTT assay findings and lactate dehydrogenase (LDH) cytotoxicity assessment. In cells exposed to nano-TiO, lycopene pretreatment significantly boosted the activity of antioxidative enzymes and reduced oxidative stress. Furthermore, when SH-SY5Y cells were subjected to nano-TiO, 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.
由于其抗氧化作用，类胡萝卜素番茄红素已被证明在多种疾病模型中具有保护作用；然而，其对纳米二氧化钛（nano-TiO）诱导的神经毒性的影响尚未确定。本研究的目的是评估番茄红素如何影响由纳米二氧化钛引起的神经元损伤及其相关机制。用不同浓度的纳米二氧化钛处理SH-SY5Y细胞48小时，之后使用MTT（3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐）试验评估细胞活力。确定了纳米二氧化钛的半数抑制浓度（IC），结果显示IC等于40µM/mL，在暴露于40µM纳米二氧化钛前一小时，将番茄红素（10µM）应用于SH-SY5Y人神经母细胞瘤细胞。测量活性氧、脂质过氧化、一氧化氮、谷胱甘肽、超氧化物歧化酶和过氧化氢酶、肿瘤坏死因子-α、白细胞介素1β、核因子κB以及凋亡标志物（Bcl2、Bax和半胱天冬酶-3），以确定番茄红素的抗氧化作用。根据MTT试验结果和乳酸脱氢酶（LDH）细胞毒性评估，在SH-SY5Y神经母细胞瘤细胞中，用10µM番茄红素预处理可显著降低暴露于纳米二氧化钛所带来的毒性。在暴露于纳米二氧化钛的细胞中，番茄红素预处理可显著提高抗氧化酶的活性并降低氧化应激。此外，当SH-SY5Y细胞暴露于纳米二氧化钛时，番茄红素预处理可阻止神经炎症和细胞凋亡。本研究结果表明，番茄红素可能是一种有效的抗氧化应激和神经炎症的神经保护剂，可用于阻止各种神经系统疾病中的神经元死亡或损伤。
