Antioxidative Effects of Cherry Leaves Extract on tert-Butyl Hydroperoxide-Mediated Cytotoxicity Through Regulation of Thioredoxin-2 Protein Expression Levels

Antioxidative Effects of Cherry Leaves Extract on tert-Butyl Hydroperoxide-Mediated Cytotoxicity Through Regulation of Thioredoxin-2 Protein Expression Levels
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樱桃叶提取物通过调节硫氧还蛋白-2 蛋白表达水平对叔丁基过氧化氢介导的细胞毒性的抗氧化作用

DOI:
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发表时间:
2011
期刊:
Journal of Toxicology and Environmental Health, Part A
影响因子:
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通讯作者:
Masashi Kato
Masashi Kato
中科院分区:
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文献类型:
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作者:
Nobuhiko Taguchi;Noriyuki Uemura;Yuji Goto;M. Sakura;Kazuhiro Hara;M. Niwa;Machiko Iida;T. Yanagishita;D. Watanabe;Masashi Kato

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樱桃树的成分已被用作治疗各种疾病的传统草药。已知这些成分具有抗氧化作用。然而,樱桃树成分介导的抗氧化作用的机制仍然是未知的。本研究以樱桃叶提取物(CLE)为研究对象,探讨了CLE对过氧化叔丁基(t-BOOH)诱导的黑色素细胞死亡伴DNA损伤的作用机制。有趣的是,CLE通过减少DNA损伤、p38激酶激活和活性氧(ROS)产生来阻止t- boo诱导的细胞死亡。硫氧还蛋白(Trx)系统抑制剂可阻止cle介导的细胞死亡抑制,减少DNA损伤、p38激酶活性和ROS产生,而谷胱甘肽(GSH)系统抑制剂则不能。最后,数据显示CLE阻止了t- boo诱导的Trx2的减少,但不阻止Trx1和Trx还原酶(TrxR1和TrxR2)蛋白的表达。因此,我们的研究结果表明,CLE可阻止t- boo诱导的Trx2表达降低、ROS生成促进、p38激酶激活和DNA损伤增加,并可防止细胞死亡。
Components of cherry trees have been used as traditional herbal remedies for various diseases. These components are known to possess antioxidative effects. However, the mechanisms underlying cherry tree component-mediated antioxidative effects remain largely unknown. This study focused on cherry leaves extract (CLE) and examined the mechanism underlying the effect of CLE on tert-butyl hydroperoxide (t-BOOH)-induced melanocytic cell death with DNA damage. Interestingly, CLE prevented t-BOOH-induced cell death with reduction in DNA damage, p38 kinase activation, and reactive oxygen species (ROS) production. CLE-mediated suppression of cell death with reduction of DNA damage, p38 kinase activity and ROS production was prevented by a thioredoxin (Trx) system inhibitor but not by a glutathione (GSH) system inhibitor. Finally, data showed that CLE prevented t-BOOH-induced reduction of Trx2 but not Trx1 and Trx reductases (TrxR1 and TrxR2) protein expression. Thus, our results suggest that CLE prevents t-BOOH-induced reduction in Trx2 expression, promotion of ROS production, activation of p38 kinase, and increase in DNA damage and that it protects against cell death.
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抗氧化剂抑制 LLC-PK1 细胞中碘乙酰胺和叔丁基氢过氧化物的毒性:脂质过氧化在烷基化诱导的细胞毒性中的作用。
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