• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >N-acetylcysteine attenuates TNF-alpha induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes
【24h】

N-acetylcysteine attenuates TNF-alpha induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes

机译：N-乙酰半胱氨酸可减轻TNF-α诱导的3T3-L1脂肪细胞分泌白介素6，纤溶酶原激活物抑制剂1和脂联素分泌的变化

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

TNF-alpha is a key molecule in obesity-related metabolic disturbances. This study was designed to determine whether N-acetylcysteine (NAC), an antioxidant, prevents the activation of nuclear factor-kappa B (NF-kappa B) by exogenously administered TNF-alpha in adipocytes, and whether such change affects the production of adipocytokines. The treatment of well-differentiated 3T3-L1 cells with 20 mM of NAC significantly increased the reduced glutathione concentration up to 150% of control. The treatment with 10 ng/ml of TNF-alpha decreased antioxidant enzyme levels such as CuZn-superoxide dismutase (SOD), MnSOD and catalase, and activated NF-kappa B in 3T3-L1 adipocytes. The activation of NF-kappa B was significantly prevented by the pretreatment with 20 mM of NAC. TNF-alpha (1-10 ng/ml) dose-dependently increased interleukin (IL)-6 and plasminogen activator inhibitor-1 (PAI-1) secretion from 3T3-L1 adipocytes, while decreased adiponectin secretion. NAC (5-20 mM) attenuated the TNF-alpha-induced changes in these adipocytokine secretions in a dose-dependent manner. The effect of TNF-alpha and NAC on the adipocytokine productions was exerted at the m-RNA level, judging from results of the real time RT-PCR analysis. The present study revealed that NAC inhibited the TNF-alpha-mediated activation of NF-kappa B and improved the adverse changes in the levels of IL-6, PAI-1 and adiponectin in 3T3-L1 adipocytes. NAC may have the potential to improve the obesity-related abnormal adipocytokine metabolism by attenuating the TNF-alpha-induced oxidant-antioxidant imbalance in adipocytes. (c) 2006 Elsevier Inc. All rights reserved.
机译：TNF-α是肥胖相关代谢紊乱的关键分子。这项研究旨在确定抗氧化剂N-乙酰半胱氨酸（NAC）是否能通过在脂肪细胞中外用TNF-α来阻止核因子-κB（NF-κB）的活化，以及这种变化是否影响脂肪细胞因子的产生。用20 mM NAC处理分化良好的3T3-L1细胞可显着降低还原型谷胱甘肽浓度，最高可达对照组的150％。用10 ng / mlTNF-α的治疗降低了3T3-L1脂肪细胞中的抗氧化酶水平，例如CuZn-超氧化物歧化酶（SOD），MnSOD和过氧化氢酶，并激活了NF-κB。用20 mM NAC预处理可显着阻止NF-κB的活化。 TNF-alpha（1-10 ng / ml）剂量依赖性地增加3T3-L1脂肪细胞分泌白介素（IL）-6和纤溶酶原激活物抑制剂1（PAI-1）的分泌，而脂联素的分泌减少。 NAC（5-20​​ mM）以剂量依赖性方式减弱了这些脂肪细胞因子分泌中TNF-α诱导的变化。从实时RT-PCR分析的结果来看，TNF-α和NAC对脂肪细胞因子产生的影响在m-RNA水平上发挥。本研究表明，NAC抑制TNF-α介导的NF-κB活化，并改善3T3-L1脂肪细胞中IL-6，PAI-1和脂联素水平的不利变化。 NAC可能具有通过减轻脂肪细胞中TNF-α诱导的氧化剂-抗氧化剂失衡来改善与肥胖相关的异常脂肪细胞因子代谢的潜力。 （c）2006 Elsevier Inc.保留所有权利。

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