首页> 美国卫生研究院文献>Journal of Neuroinflammation >Omega-3 polyunsaturated fatty acid attenuates traumatic brain injury-induced neuronal apoptosis by inducing autophagy through the upregulation of SIRT1-mediated deacetylation of Beclin-1
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Omega-3 polyunsaturated fatty acid attenuates traumatic brain injury-induced neuronal apoptosis by inducing autophagy through the upregulation of SIRT1-mediated deacetylation of Beclin-1

机译:Omega-3多不饱和脂肪酸通过上调SIRT1介导的Beclin-1的自噬来诱导自噬从而减轻颅脑损伤诱导的神经元凋亡。

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摘要

BackgroundEnhancing autophagy after traumatic brain injury (TBI) may decrease the expression of neuronal apoptosis-related molecules. Autophagy-mediated neuronal survival is regulated by the sirtuin family of proteins (SIRT). Omega-3 polyunsaturated fatty acids (ω-3 PUFA) are known to have antioxidative and anti-inflammatory effects. We previously demonstrated that ω-3 PUFA supplementation attenuated neuronal apoptosis by modulating the neuroinflammatory response through SIRT1-mediated deacetylation of the HMGB1/NF-κB pathway, leading to neuroprotective effects following experimental traumatic brain injury (TBI). However, no studies have elucidated if the neuroprotective effects of ω-3 PUFAs against TBI-induced neuronal apoptosis are modulated by SIRT1-mediated deacetylation of the autophagy pathway.
机译:背景外伤性脑损伤(TBI)后增强自噬可能会降低神经元凋亡相关分子的表达。自噬介导的神经元生存是由瑟土因蛋白家族(SIRT)调节的。已知Omega-3多不饱和脂肪酸(ω-3PUFA)具有抗氧化和抗炎作用。我们先前证明,ω-3PUFA补充剂通过SIRT1介导的HMGB1 /NF-κB途径的脱乙酰基化来调节神经炎症反应,从而减轻神经元凋亡,从而导致实验性脑外伤(TBI)后的神经保护作用。然而,尚无研究阐明ω-3PUFA对TBI诱导的神经元凋亡的神经保护作用是否由SIRT1介导的自噬途径的脱乙酰作用调节。

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