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首页> 外文期刊>The Journal of Nutritional Biochemistry >Dietary flavonoid fisetin regulates aluminium chloride-induced neuronal apoptosis in cortex and hippocampus of mice brain
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Dietary flavonoid fisetin regulates aluminium chloride-induced neuronal apoptosis in cortex and hippocampus of mice brain

机译：膳食类黄酮非瑟汀调节氯化铝诱导的小鼠大脑皮层和海马神经元凋亡

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Dietary flavonoids have been suggested to promote brain health by protecting brain parenchymal cells. Recently, understanding the possible mechanism underlying neuroprotective efficacy of flavonoids is of great interest. Given that fisetin exerts neuroprotection, we have examined the mechanisms underlying fisetin in regulating A beta aggregation and neuronal apoptosis induced by aluminium chloride (AlCl3) administration in vivo. Male Swiss albino mice were induced orally with AlCl3 (200 mg/kg. b.wt./day/8 weeks). Fisetin (15 mg/Kg. b.wt. orally) was administered for 4 weeks before AlCl3-induction and administered simultaneously for 8 weeks during AlCl3-induction. We found aggregation of Amyloid beta (A beta 40-42), elevated expressions of Apoptosis stimulating kinase (ASK-1), p-JNK (c-Jun N-terminal Kinase), p53, cytochrome c, caspases-9 and 3, with altered Bax/Bcl-2 ratio in favour of apoptosis in cortex and hippocampus of AlCl3-administered mice. Furthermore, TUNEL and fluoro-jade C staining demonstrate neurodegeneration in cortex and hippocampus. Notably, treatment with fisetin significantly (P0.05) reduced A beta aggregation, ASK-1, p-JNK, p53, cytochrome c, caspase-9 and 3 protein expressions and modulated Bax/Bcl-2 ratio. TUNEL-positive and fluoro-jade C stained cells were also significantly reduced upon fisetin treatment. We have identified the involvement of fisetin in regulating ASK-1 and p-JNK as possible mediator of A beta aggregation and subsequent neuronal apoptosis during AlCl3-induced neurodegeneration. These findings define the possibility that fisetin may slow or prevent neurodegneration and can be utilised as neuroprotective agent against Alzheimer's and Parkinson's disease. (C) 2015 Elsevier Inc. All rights reserved.
机译：饮食中的类黄酮已被建议通过保护脑实质细胞来促进脑部健康。最近，了解类黄酮的神经保护功效的潜在机制引起了极大的兴趣。鉴于非瑟汀具有神经保护作用，我们已经研究了非瑟汀在调节A聚合和体内氯化铝（AlCl3）诱导的神经元凋亡中的机制。用AlCl3（200 mg / kg。b.wt./day/8周）口服诱导雄性瑞士白化病小鼠。 Fisetin（15 mg / Kg。b.wt.口服）在AlCl3诱导前给药4周，在AlCl3诱导过程中同时给药8周。我们发现了淀粉样蛋白β（A beta 40-42）的聚集，凋亡刺激激酶（ASK-1），p-JNK（c-Jun N-末端激酶），p53，细胞色素c，胱天蛋白酶9和3的表达升高，改变Bax / Bcl-2比例，有利于AlCl3所致小鼠皮质和海马的凋亡。此外，TUNEL和氟玉石C染色显示皮层和海马神经变性。值得注意的是，用非瑟定治疗显着（P <0.05）降低了Aβ聚集，ASK-1，p-JNK，p53，细胞色素c，caspase-9和3蛋白表达，并调节了Bax / Bcl-2比率。进行非瑟定素处理后，TUNEL阳性和氟玉石C染色的细胞也明显减少。我们已经确定了非瑟酮在调节ASK-1和p-JNK中的作用，这可能是AlCl3诱导的神经变性期间Aβ聚集和随后神经元凋亡的媒介。这些发现确定了非瑟定可能减慢或预防神经退化的可能性，并可用作抗阿尔茨海默氏病和帕金森氏病的神经保护剂。 （C）2015 Elsevier Inc.保留所有权利。

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