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双黄酮-考维酮可保护人多巴胺能 SH-SY5Y 细胞免受莠去津诱导的毒性损伤。

Biflavanone-kolaviron protects human dopaminergic SH-SY5Y cells against atrazine induced toxic insult.

机构信息

Department of Chemical Sciences, College of Natural Sciences, Redeemer's University, Redemption City, Ogun State, Nigeria.

出版信息

Toxicol In Vitro. 2011 Jun;25(4):848-58. doi: 10.1016/j.tiv.2011.02.005. Epub 2011 Feb 17.

DOI:10.1016/j.tiv.2011.02.005
PMID:21333729
Abstract

Atrazine (ATR) is a widespread agrochemical contaminant frequently detected in water systems and kolaviron (KV) is a seed-derived biflavonoid which is reported to modulate the effects of many mutagens and carcinogens. We investigated the protective effects of KV on ATR-induced cell death in the human neuroblastoma cell line (SHY-SY5Y). KV prevents ATR-induced generation of reactive oxygen species (ROS), cell death and inhibited cell proliferation by reduction of cell proliferation. Further, ATR-induced levels malondialdehyde (MDA), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR) activities, increased leakage of lactate dehydrogenase (LDH), inhibited cellular LDH activity and depleted glutathione (GSH) levels in SHY-SY5Y cells were blocked by KV. Comparable to the control, KV increased GR but not GSH-Px activities. ATR mediated nuclear changes associated with apoptosis; including nuclear fragmentation, condensation, DNA laddering, and increased caspase-3 activity were blocked on addition of KV. ATR-induced changes in the expressions of p53, Bax, Bcl-2, p21, and mRNA levels of caspase-3 and caspase-9 were prevented by KV. Based on these results, we propose a model for the protective effect of KV on ATR-induced cell injury in neuronal cell.

摘要

莠去津(ATR)是一种广泛存在的农用化学品污染物,经常在水系统中检测到,而 kolaviron(KV)是一种从种子中提取的双黄酮类化合物,据报道可以调节许多诱变剂和致癌剂的作用。我们研究了 KV 对 ATR 诱导的人神经母细胞瘤细胞系(SHY-SY5Y)细胞死亡的保护作用。KV 可防止 ATR 诱导的活性氧(ROS)生成、细胞死亡,并通过减少细胞增殖来抑制细胞增殖。此外,ATR 诱导的丙二醛(MDA)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽还原酶(GR)活性增加、乳酸脱氢酶(LDH)漏出增加、细胞内 LDH 活性抑制和细胞内 GSH 水平降低在 SHY-SY5Y 细胞中被 KV 阻断。与对照组相比,KV 增加了 GR 但没有增加 GSH-Px 活性。ATR 介导的与细胞凋亡相关的核变化;包括核片段化、浓缩、DNA 梯化和 caspase-3 活性增加,在添加 KV 后被阻断。ATR 诱导的 p53、Bax、Bcl-2、p21 的表达变化以及 caspase-3 和 caspase-9 的 mRNA 水平也被 KV 阻止。基于这些结果,我们提出了 KV 对 ATR 诱导神经元细胞损伤的保护作用模型。

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