首页> 外文期刊>Life sciences >Overexpression of phospholipase C beta-1 protects NIH3T3 cells from oxidative stress-induced cell death
【24h】

Overexpression of phospholipase C beta-1 protects NIH3T3 cells from oxidative stress-induced cell death

机译:磷脂酶C beta-1的过表达保护NIH3T3细胞免受氧化应激诱导的细胞死亡

获取原文
获取原文并翻译 | 示例
           

摘要

Oxidative stress has been implicated in a wide range of cellular damage which includes DNA oxidation, membrane lipid peroxidation, and apoptosis. In our study, we found that overexpression of PLC-beta 1 in NIH3T3 fibroblasts protected them from cell death occuring in response to oxidative stress. Cell death caused by treatment with prooxidant tert-butylhydroperoxide (TBH), H2O2, or CdCl2 was considerably suppressed in PLC-beta 1 overexpressed NIH/beta 1-14 cells in comparison to control NIHeo cells. However, overexpression of PLC-beta 1 failed to protect the cells from toxicity by diamide or KCN. In addition, while accumulation of c-fos mRNA was observed within 30 min of TBH treatment in vector transfected NIHeo cells, TBH-induced c-fos mRNA generation was completely suppressed in NIH/beta 1-14 cells, while that of c-jun and GAPDH was not affected. These findings suggest that PLC-beta 1 may play a role in process that can protect cells from oxidative stress-induced cell death. (C) 2000 Elsevier Science Inc. All rights reserved. [References: 50]
机译:氧化应激与广泛的细胞损伤有关,包括DNA氧化,膜脂质过氧化和细胞凋亡。在我们的研究中,我们发现NIH3T3成纤维细胞中PLC-beta 1的过表达保护它们免受因氧化应激而发生的细胞死亡。与对照NIH / neo细胞相比,在PLC-beta 1过表达的NIH / beta 1-14细胞中,用抗氧化剂叔丁基过氧化氢(TBH),H2O2或CdCl2处理引起的细胞死亡被大大抑制。但是,PLC-beta 1的过表达不能保护细胞免受二酰胺或KCN的毒性。此外,虽然在载体转染的NIH / neo细胞中,在TBH处理后30分钟内观察到了c-fos mRNA的积累,但在NIH / beta 1-14细胞中,TBH诱导的c-fos mRNA的生成被完全抑制了,而c -jun和GAPDH不受影响。这些发现表明,PLC-beta 1可能在保护细胞免受氧化应激诱导的细胞死亡的过程中起作用。 (C)2000 Elsevier Science Inc.保留所有权利。 [参考:50]

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号