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氯化矢车菊素可能通过诱导自噬,适度保护 Caco-2 细胞免受 ZnO 纳米颗粒的暴露。

Cyanidin chloride modestly protects Caco-2 cells from ZnO nanoparticle exposure probably through the induction of autophagy.

机构信息

Institute of Bast Fiber Crops, Chinese Academy of Agricultural Sciences, Changsha, 410205, PR China; Key Laboratory of Environment-Friendly Chemistry and Applications of Ministry Education, Laboratory of Biochemistry, College of Chemistry, Xiangtan University, Xiangtan, 411105, PR China.

Key Laboratory of Environment-Friendly Chemistry and Applications of Ministry Education, Laboratory of Biochemistry, College of Chemistry, Xiangtan University, Xiangtan, 411105, PR China.

出版信息

Food Chem Toxicol. 2019 May;127:251-259. doi: 10.1016/j.fct.2019.03.047. Epub 2019 Mar 26.

DOI:10.1016/j.fct.2019.03.047
PMID:30922967
Abstract

Recent studies suggest that phytochemicals, as part of the food matrix, might alter the toxicity of nanoparticles (NPs); however, relatively few studies have investigated the impact of anthocyanidins on the toxicity of NPs to cells lining the gastrointestinal tract. Therefore, this study used cyanidin chloride (CC) as the model for anthocyanidins and investigated the effects of CC on the toxicity of ZnO or Ag NPs to Caco-2 cells. Exposure to ZnO but not Ag NPs significantly induced cytotoxicity. The presence of CC, but not its analog quercetin (Qu), modestly protected Caco-2 cells from ZnO NP exposure. However, the intracellular superoxide, Zn ions, or release of interleukin-8 after ZnO NP exposure were not significantly affected by the presence of CC. Rather, CC promoted the expression of autophagic genes ATG5, ATG7, and BECN1 as well as the ratio of LC3-II/I after exposure to ZnO NPs. Meanwhile, the presence of autophagic inhibitors (chloroquine, NHCl, bafilomycin A1) significantly promoted the cytotoxicity of ZnO NPs and inhibited the cytoprotective effects of CC. In conclusion, these data suggest that CC could modestly protect Caco-2 cells from ZnO NP exposure, probably through the induction of autophagy.

摘要

最近的研究表明,植物化学物质作为食物基质的一部分,可能会改变纳米颗粒(NPs)的毒性;然而,相对较少的研究调查了花色苷对纳米颗粒对胃肠道衬里细胞毒性的影响。因此,本研究使用氰花翠(CC)作为花色苷的模型,研究了 CC 对 ZnO 或 Ag NPs 对 Caco-2 细胞毒性的影响。暴露于 ZnO 但不是 Ag NPs 显著诱导了细胞毒性。CC 的存在,但不是其类似物槲皮素(Qu),适度保护 Caco-2 细胞免受 ZnO NP 暴露。然而,CC 对暴露于 ZnO NPs 后细胞内超氧阴离子、Zn 离子或白细胞介素-8 的释放没有显著影响。相反,CC 促进了自噬基因 ATG5、ATG7 和 BECN1 的表达以及 LC3-II/I 的比值在暴露于 ZnO NPs 后。同时,自噬抑制剂(氯喹、NHCl、巴弗洛霉素 A1)的存在显著促进了 ZnO NPs 的细胞毒性,并抑制了 CC 的细胞保护作用。总之,这些数据表明 CC 可以适度保护 Caco-2 细胞免受 ZnO NP 暴露,可能是通过诱导自噬。

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