首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Protective effects of lycopene against amyloid beta-induced neurotoxicity in cultured rat cortical neurons.
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Protective effects of lycopene against amyloid beta-induced neurotoxicity in cultured rat cortical neurons.

机译:番茄红素对淀粉样β诱导的大鼠皮质神经元神经毒性的保护作用。

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摘要

The neurotoxicity of amyloid beta (Abeta) has been implicated as a critical cause in the pathogenesis of Alzheimer's disease (AD). Among antioxidant phytochemicals derived from fruit and vegetables, lycopene has recently received considerable attention for its potent protective properties already demonstrated in several models of oxidative damage. The present study aims to investigate whether lycopene could provide protective effects against Abeta-induced neurotoxicity in primary cultured rat cortical neurons. The cultured cortical neurons were pretreated with different dose of lycopene for 4h, followed by the challenge with 25 muM Abeta(25-35) for 24h. The results showed that pretreatment with lycopene efficiently attenuated Abeta(25-35)-induced neurotoxicity, as evidenced by the improved cell viability and the decreased apoptotic rate. In addition, lycopene inhibited the reactive oxygen species generation and mitochondrial membrane potential depolarization caused by Abeta(25-35). Lycopene also restored the levels of proapoptotic Bax, antiapoptotic Bcl-2, and inhibited caspase-3 activation. These beneficial effects may contribute to the protection against Abeta-induced neurotoxicity. Together, our results suggest that the natural antioxidant lycopene has potential for neuroprotection and therefore, may be a promising candidate for AD treatment.
机译:淀粉样β(Abeta)的神经毒性已被认为是阿尔茨海默氏病(AD)发病机理中的关键原因。在源自水果和蔬菜的抗氧化剂植物化学物质中,番茄红素因其在多种氧化损伤模型中已证明的有效保护特性而受到了广泛关注。本研究旨在调查番茄红素是否可以对原代培养的大鼠皮质神经元中的Abeta诱导的神经毒性提供保护作用。培养的皮质神经元用不同剂量的番茄红素预处理4h,然后用25μMAbeta(25-35)攻击24h。结果表明,番茄红素预处理有效地减弱了Abeta(25-35)诱导的神经毒性,这可以通过改善细胞活力和降低凋亡率来证明。此外,番茄红素抑制由Abeta(25-35)引起的活性氧的产生和线粒体膜电位的去极化。番茄红素还恢复了凋亡前Bax,抗凋亡Bcl-2的水平,并抑制了caspase-3的活化。这些有益的作用可能有助于防止Abeta诱导的神经毒性。总之,我们的结果表明,天然抗氧化剂番茄红素具有潜在的神经保护作用,因此,可能是有希望的AD治疗候选药物。

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