Taurine attenuates acrylamide-induced apoptosis via a PI3K/AKT-dependent manner

被引:17
作者
Sun, G. [1 ]
Wang, X. [1 ]
Li, T. [1 ]
Qu, S. [2 ]
Sun, J. [1 ]
机构
[1] Dalian Med Univ, Affiliated Hosp 1, Dalian 116011, Liaoning, Peoples R China
[2] Dalian Med Univ, Inst Canc Stem Cell, Dalian, Liaoning, Peoples R China
基金
中国国家自然科学基金;
关键词
Taurine; acrylamide; apoptosis; PI3K/AKT-dependent manner; EPOXIDE METABOLITE; PRIMARY ASTROCYTES; NEUROTOXICITY; GLYCIDAMIDE; NEUROPATHY; CASPASE-3; TOXICITY; BCL-2; HIPPOCAMPAL; INHIBITION;
D O I
10.1177/0960327118765335
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
As a potent neurotoxic agent, acrylamide (ACR) is formed in food processing at higher temperature. Taurine (TAU), a nonessential amino acid, is used to cure neurodegenerative disorders, followed by activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. In this article, we certified that antiapoptotic efficacy of TAU in vivo and vitro. ACR-treated rats received TAU by drinking water 2 weeks after ACR intoxication. The results showed that in treated rats, TAU alleviated ACR-induced neuronal apoptosis, which was associated with the activation of PI3K/AKT signaling pathway. TAU attenuated apoptosis caused by ACR through observing terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells, measure of protein expression of Bcl-2, Bax, and caspase 3 activity. TAU-induced antiapoptotic effect is PI3K/AKT-dependent, which was proved in ACR-intoxicated ventral spinal cord 4.1 cells in the presence of AKT inhibitor, MK-2206. Therefore, our results demonstrated that TAU-attenuated ACR-induced apoptosis in vivo through a PI3K/AKT-dependent manner provided new sights in the molecular mechanism of TAU protection against ACR-induced neurotoxicity.
引用
收藏
页码:1249 / 1257
页数:9
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