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Apigenin and its octoic acid diester attenuated glycidol-induced autophagic-dependent apoptosis via inhibiting the ERK/JNK/p38 signaling pathways in human umbilical vein endothelial cells (HUVECs)

文献类型： 外文期刊

作者： Zhao, Yue 1 ; Jiang, Qingqing 1 ; Guo, Limin 3 ; Fan, Daming 4 ; Wang, Mingfu 5 ; Zhao, Yueliang 1 ;

作者机构： 1.Shanghai Ocean Univ, Coll Food Sci & Technol, Shanghai 201306, Peoples R China

2.Minist Agr, Lab Qual & Safety Risk Assessment Aquat Prod Stora, Shanghai 201306, Peoples R China

3.Xinjiang Acad Agr Sci, Inst Agroprod Storage & Proc, Urumqi 830091, Peoples R China

4.Jiangnan Univ, Sch Food Sci & Technol, Wuxi, Peoples R China

5.Shenzhen Univ, Inst Adv Study, Shenzhen, Peoples R China

6.Shanghai Ocean Univ, Coll Food Sci & Technol, Shanghai, Peoples R China

关键词： Glycidol; Autophagy; Apoptosis; Apigenin; Mitogen-activated protein kinase (MAPK); MAPK signaling Pathway

期刊名称：CURRENT RESEARCH IN FOOD SCIENCE （ 影响因子：6.3； 五年影响因子：6.3 ）

ISSN：

年卷期： 2023 年 6 卷

页码：

收录情况： SCI

摘要： Glycidol is a well-known food contaminant mainly formed in refined edible oils and various thermally processed foods. Here, we studied the toxicity effects and related mechanism of glycidol on Human umbilical vein endothelial cells (HUVECs). Glycidol was found to induce Gap period 2 (G2)/Mitosis (M) phase cell cycle arrest, apoptosis, and autophagy in HUVECs. Inhibition of autophagy by 3-methyladenine (3-MA) attenuated glycidolinduced cell death, suggesting that glycidol-induced apoptosis was autophagy-dependent. Moreover, glycidol treatment induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal protein kinase (JNK), and p38. Inhibition of ERK, JNK, and p38 phosphorylation by the inhibitors U0126, SP600125, and SB203580 attenuated glycidol-induced autophagy and prevented glycidol-mediated reduction in cell viability, demonstrating that glycidol inhibited HUVECs growth by inducing autophagic-dependent apoptosis through activation of the ERK, JNK and p38 signaling pathways. In addition, apigenin (API) and its octoic acid diester apigenin-7 (API-C8), 4 '-O-dioctanoate were found to significantly attenuate glycidol-induced cell growth inhibition by inhibiting the above signaling pathways. Collectively, glycidol induces autophagic-dependent apoptosis via activating the ERK/JNK/p38 signaling pathways in HUVECs and API-C8 could attenuate the toxicity effects.

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