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Neuroprotective effects of chloroform and aqueous fractions of noni juice against t-Butyl hydroperoxide-induced oxidative damage in SH-SY5Y cells

机译:氯仿和诺丽果汁水部分对叔丁基过氧化氢诱导的SH-SY5Y细胞氧化损伤的神经保护作用

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摘要

Oxidative stress is more likely to cause damage to neuronal cells and mediates some neurodegenerative disorders. It is well known that natural antioxidants can prevent oxidative stress damage and become a potential therapeutic strategy. Noni juice obtained from the fruit of the tree Morinda citrifolia, as a folk medicine, has been used for over two thousand years. In the current study, the neuroprotective effect and mechanism of noni juice extracts against tert-Butyl hydroperoxide (TBHP)-induced SH-SY5Y cell damage were investigated. The results demonstrated that chloroform fraction (CF) and aqueous fraction (AF) of noni juice protected SH-SY5Y cells against TBHP-induced oxidative stress and the associated apoptosis effectively. CF and AF treatment significantly weakened the TBHP-induced cytotoxicity, reactive oxygen species generation, mitochondrial membrane depolarization, and apoptotic features. CF and AF restored cellular antioxidant enzyme activity; upregulated expression of heme oxygenase-1, catalase, and superoxide dismutase-1; and increased the nuclear accumulation of nuclear factor-erythroid 2 related factor 2 (Nrf2). The antioxidant and neuroprotection potential of CF may account for its high total phenolic and flavonoid content, while AF may be rich in polysaccharides. These results suggest that CF and AF exhibit antioxidant defense through the upregulation of Nrf2 along with endogenous antioxidants and reduce apoptosis via inhibiting the mitochondrial pathway to protect SH-SY5Y cells damaged by TBHP. CF and AF might be developed as agents for neurodegeneration prevention or therapy.
机译:氧化应激更可能导致神经元细胞受损并介导一些神经退行性疾病。众所周知,天然抗氧化剂可以防止氧化应激损伤并成为潜在的治疗策略。从树巴戟天的果实中获得的诺丽汁作为一种民间药物已使用了两千多年。在当前的研究中,研究了诺丽汁提取物对叔丁基氢过氧化物(TBHP)诱导的SH-SY5Y细胞损伤的神经保护作用和机制。结果表明,诺丽汁的氯仿级分(CF)和水级分(AF)保护SH-SY5Y细胞免受TBHP诱导的氧化应激和相关的细胞凋亡。 CF和AF治疗显着削弱了TBHP诱导的细胞毒性,活性氧生成,线粒体膜去极化和凋亡功能。 CF和AF恢复了细胞抗氧化酶的活性;血红素加氧酶-1,过氧化氢酶和超氧化物歧化酶-1的表达上调;并增加了核因子-类胡萝卜素2相关因子2(Nrf2)的核积累。 CF的抗氧化剂和神经保护能力可能是其总酚和类黄酮含量高的原因,而AF可能富含多糖。这些结果表明,CF和AF通过与内源性抗氧化剂一起上调Nrf2来发挥抗氧化防御作用,并通过抑制线粒体途径来保护被TBHP破坏的SH-SY5Y细胞,从而减少细胞凋亡。 CF和AF可能被开发为预防或治疗神经退行性疾病的药物。

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