• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of neuroinflammation >TSG (2,3,4’?,5-tetrahydroxystilbene 2-O-β-D-glucoside) suppresses induction of pro-inflammatory factors by attenuating the binding activity of nuclear factor-κB in microglia
【24h】

TSG (2,3,4’?,5-tetrahydroxystilbene 2-O-β-D-glucoside) suppresses induction of pro-inflammatory factors by attenuating the binding activity of nuclear factor-κB in microglia

机译：TSG（2,3,4'？，5-四羟基sti2-O-β-D-葡萄糖苷）通过减弱小胶质细胞核因子-κB的结合活性来抑制促炎因子的诱导

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Background Induction of pro-inflammatory factors is one of the characteristics of microglia activation and can be regulated by numerous active components of Chinese traditional herbs. Suppression of pro-inflammatory factors is beneficial to alleviate microglia-mediated cell injury. The present study aims to investigate the effect and possible mechanism of 2,3,4鈥?5-tetrahydroxystilbene 2-O-尾-D-glucoside (TSG) on LPS-mediated induction of pro-inflammatory factors in microglia. Methods Western blot, ELISA, and Hoechst 33258 were used to measure the protein expression, TNF-伪/IL-6 content, and apoptotic nuclei, respectively. The mRNA level was measured by real time-PCR. Nitric oxide (NO) content, lactate dehydrogenase (LDH) content, and NF-魏B binding activity were assayed by commercial kits. Results TSG reduced iNOS protein expression as well as TNF-伪, IL-6, and NO content in LPS-stimulated BV-2 cells. TSG attenuated the increase in apoptotic nuclei, caspase-3 cleavage, and LDH content induced by BV-2 cell-derived conditioned medium in primary hippocampal neurons. Mechanistic studies showed that TSG reduced the mRNA level of iNOS, TNF-伪, and IL-6. TSG failed to suppress I魏B-伪 degradation, NF-魏B phosphorylation and nuclear translocation, and ERK1/2, JNK, and p38 phosphorylation. TSG, however, markedly reduced the binding of NF-魏B to its DNA element. Chromatin immunoprecipitation (ChIP) assays confirmed that TSG reduced NF-魏B binding to the iNOS promoter. These findings were ascertained in primary microglia where the LPS-induced increase in iNOS expression, NO content, apoptotic nuclei, and NF-魏B binding to its DNA element were diminished by TSG. Conclusions These studies demonstrate that TSG attenuates LPS-mediated induction of pro-inflammatory factors in microglia through reducing the binding activity of NF-魏B. This might help us to further understand the pharmacological role of TSG in inflammatory response in the central nervous system.
机译：背景促炎因子的诱导是小胶质细胞活化的特征之一，并且可以由中药的许多活性成分调节。抑制促炎因子有利于减轻小胶质细胞介导的细胞损伤。本研究旨在探讨2,3,4'5-四羟基sti2-O-β-D-葡萄糖苷（TSG）对LPS介导的小胶质细胞促炎因子的诱导作用及其可能的机制。方法分别用蛋白质印迹法，ELISA法和Hoechst 33258法检测蛋白表达，TNF-α/ IL-6含量和凋亡细胞核。通过实时PCR测量mRNA水平。一氧化氮（NO）含量，乳酸脱氢酶（LDH）含量和NF-魏布结合活性通过商业试剂盒进行了测​​定。结果TSG降低了LPS刺激的BV-2细胞中的iNOS蛋白表达以及TNF-α，IL-6和NO含量。 TSG减弱了原代海马神经元中BV-2细胞来源的条件培养基诱导的凋亡核，caspase-3裂解和LDH含量的增加。机理研究表明，TSG降低了iNOS，TNF-α和IL-6的mRNA水平。 TSG无法抑制I魏B-α降解，NF-魏B磷酸化和核易位以及ERK1 / 2，JNK和p38磷酸化。但是，TSG明显降低了NF-魏布与其DNA元素的结合。染色质免疫沉淀（ChIP）分析证实，TSG减少了NF-魏布与iNOS启动子的结合。这些发现是在原发性小胶质细胞中确定的，其中TPS降低了LPS诱导的iNOS表达，NO含量，凋亡核和NF-魏布与其DNA元素结合的增加。结论这些研究表明，TSG通过降低NF-魏布的结合活性来减弱LPS介导的小胶质细胞促炎因子的诱导。这可能有助于我们进一步了解TSG在中枢神经系统炎症反应中的药理作用。

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