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表没食子儿茶素-3-没食子酸酯减轻丙烯酰胺诱导的大鼠大脑皮质细胞凋亡和星形胶质细胞增生。

Epigallocatechin-3-gallate attenuates acrylamide-induced apoptosis and astrogliosis in rat cerebral cortex.

作者信息

He Yin, Tan Dehong, Bai Bing, Wu Zhaoxia, Ji Shujuan

机构信息

a College of Food , Shenyang Agricultural University , Shenhe District , Shenyang City , People's Republic of China.

出版信息

Toxicol Mech Methods. 2017 May;27(4):298-306. doi: 10.1080/15376516.2017.1279251. Epub 2017 Jan 22.

Abstract

The potent neurotoxic agent acrylamide (ACR) is formed during Maillard reaction in food processing. Epigallocatechin-3-gallate (EGCG), a major bioactive component of green tea, is an antioxidant, but its effects on ACR-induced neurotoxicity are unclear. Here, we investigated the neuroprotective effects of EGCG against ACR-induced apoptosis and astrogliosis in the cerebral cortex. Rats were pretreated with EGCG for 4 d and then co-administered ACR for 14 d. Immunohistochemical analysis of glial fibrillary acidic protein and 8-hydroxy-2'-deoxyguanosine indicated that EGCG attenuated astrogliosis and DNA damage in ACR-treated rats. Analysis of DNA fragmentation and protein expression of Bax, Bcl-2, caspase 3, and cytochrome c revealed that EGCG inhibited ACR-induced apoptosis. Furthermore, EGCG inhibited oxidative stress by enhancing the activity of antioxidant enzymes and glutathione levels and reducing the formation of reactive oxygen species and lipid peroxidation. Taken together, our data demonstrate that EGCG inhibits ACR-induced apoptosis and astrogliosis in the cerebral cortex.

摘要

强效神经毒剂丙烯酰胺(ACR)在食品加工的美拉德反应过程中形成。表没食子儿茶素-3-没食子酸酯(EGCG)是绿茶的主要生物活性成分,是一种抗氧化剂,但其对ACR诱导的神经毒性的影响尚不清楚。在此,我们研究了EGCG对ACR诱导的大脑皮质细胞凋亡和星形胶质细胞增生的神经保护作用。大鼠用EGCG预处理4天,然后与ACR共同给药14天。对胶质纤维酸性蛋白和8-羟基-2'-脱氧鸟苷进行免疫组织化学分析表明,EGCG减轻了ACR处理大鼠的星形胶质细胞增生和DNA损伤。对DNA片段化以及Bax、Bcl-2、半胱天冬酶3和细胞色素c的蛋白质表达分析显示,EGCG抑制了ACR诱导的细胞凋亡。此外,EGCG通过增强抗氧化酶的活性和谷胱甘肽水平以及减少活性氧的形成和脂质过氧化来抑制氧化应激。综上所述,我们的数据表明EGCG抑制ACR诱导的大脑皮质细胞凋亡和星形胶质细胞增生。

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