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摘要:Acrylamide(ACR) has obvious neurotoxicity in human by causing apoptosis, endoplasmic reticulum stress, and autophagy, but the relationships among were still unclear. This study aimed to investigate the roles of ERS and autophagy in vitro, to further demonstrate the mechanism of ACR neurotoxicity. In present study, different doses of ACR were set, to value ACR toxicity, then the PERK inhibitor and autophagy inhibitor, GSK2606414 and 3-Methyladenine, were used separately to inhibit ERS and autophagy activation under ACR treatment. With the increases of ACR dose, the cell viability and apoptotic rate dose-dependently decreased. After ERS inhibition, the apoptosis and autophagy caused by ACR were alleviated, showing reduced apoptotic rate, and down-regulated levels of Bax, Beclin1, LC3-Ⅱ/LC3-Ⅰ. While the autophagy inhibition deteriorated apoptosis, with up-regulated apoptotic rate, and increased Bax, indicating ACR caused autophagy by activating PERK pathway of ERS, and induced apoptosis finally. This study helps to provide experimental basis for exploring potential molecular targets for the prevention and control of ACR toxicity.
会议名称:

第九届亚洲毒理学大会暨中国毒理学会第八次中青年科技论坛

会议时间:

2021-10-20

会议地点:

中国浙江杭州

  • 专辑:

    医药卫生科技

  • 专题:

    药学

  • DOI:

    10.26914/c.cnkihy.2021.052455

  • 分类号:

    R99

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