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

被引：39
作者：
He, Yin [1 ]
Tan, Dehong [1 ]
Bai, Bing [1 ]
Wu, Zhaoxia [1 ]
Ji, Shujuan [1 ]
机构：
[1] Shenyang Agr Univ, Coll Food, 120 Dongling Rd, Shenyang 110866, Peoples R China
来源：
TOXICOLOGY MECHANISMS AND METHODS | 2017年 / 27卷 / 04期
基金：
中国国家自然科学基金;
关键词：
Acrylamide; epigallocatechin-3-gallate; apoptosis; astrogliosis; oxidative stress; CYTOCHROME-C; OXIDATIVE STRESS; PC12; CELLS; MITOCHONDRIA; BCL-2; NEUROTOXICITY; DEGENERATION; CASPASE-3; DEATH;
D O I：
10.1080/15376516.2017.1279251
中图分类号：
R99 [毒物学（毒理学）];
学科分类号：
100405 ;
摘要：
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-20-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.
引用
收藏
页码：298 / 306
页数：9
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