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表没食子儿茶素-3-没食子酸酯减轻丙烯酰胺处理大鼠的大脑皮质损伤并促进脑再生。

Epigallocatechin-3-gallate attenuates cerebral cortex damage and promotes brain regeneration in acrylamide-treated rats.

作者信息

He Yin, Tan Dehong, Mi Yan, Zhou Qian, Ji Shujuan

机构信息

College of Food, Shenyang Agricultural University, No. 120 Dongling Road, Shenhe District, Shenyang City 110866, People's Republic of China.

出版信息

Food Funct. 2017 Jun 21;8(6):2275-2282. doi: 10.1039/c6fo01823h.

Abstract

Acrylamide (ACR) is a neurotoxic industrial chemical intermediate, which is also present in food and water. We investigated the neuroprotective effects of epigallocatechin-3-gallate (EGCG), the most abundant polyphenol in green tea, on ACR-treated rat brain. Rats were pre-treated with EGCG for 4 d and then administered ACR and EGCG for 14 d. EGCG increased acetylcholinesterase (AChE) activity and the rate of Nissl-positive cells in ACR-treated rats. Senescence-associated β-galactosidase (SA-β-gal) staining indicated that EGCG attenuated ACR-induced senescence. Tumour necrosis factor alpha (TNF-α), inducible nitric oxide synthase (iNOS), and cyclooxygenase 2 (COX-2) protein expression indicated that EGCG inhibited ACR-induced inflammation. In addition, immunohistochemical analysis of nestin and brain-derived neurotrophic factor (BDNF) revealed that EGCG promoted brain regeneration in ACR-treated rats. Altogether, our results suggest that EGCG can attenuate ACR-induced brain damage and promote regeneration in the cerebral cortex of rats. Therefore, we hypothesized that EGCG may alleviate ACR-related nerve injury.

摘要

丙烯酰胺(ACR)是一种具有神经毒性的工业化学中间体,在食品和水中也有存在。我们研究了绿茶中含量最丰富的多酚表没食子儿茶素没食子酸酯(EGCG)对经ACR处理的大鼠大脑的神经保护作用。大鼠先用EGCG预处理4天,然后给予ACR和EGCG 14天。EGCG增加了经ACR处理的大鼠的乙酰胆碱酯酶(AChE)活性和尼氏阳性细胞的比例。衰老相关β-半乳糖苷酶(SA-β-gal)染色表明EGCG减轻了ACR诱导的衰老。肿瘤坏死因子α(TNF-α)、诱导型一氧化氮合酶(iNOS)和环氧化酶2(COX-2)蛋白表达表明EGCG抑制了ACR诱导的炎症。此外,对巢蛋白和脑源性神经营养因子(BDNF)的免疫组织化学分析显示EGCG促进了经ACR处理的大鼠的脑再生。总之,我们的结果表明EGCG可以减轻ACR诱导的脑损伤并促进大鼠大脑皮层的再生。因此,我们推测EGCG可能减轻与ACR相关的神经损伤。

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