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丹皮酚对脂多糖/三磷酸腺苷诱导的小胶质细胞NLRP3炎症小体激活的影响

王伟 戴敏 徐忠东

中国药理学通报Issue(5):652-656,5.
中国药理学通报Issue(5):652-656,5.DOI:10.3969/j.issn.1001-1978.2014.05.014

丹皮酚对脂多糖/三磷酸腺苷诱导的小胶质细胞NLRP3炎症小体激活的影响

Effects of paeonol on lipopolysaccharide/adenosine 5′-triphosphate induced NLRP3 inflammasome activation in primary rat microglia

王伟 1戴敏 2徐忠东1

作者信息

  • 1. 合肥师范学院生命科学系,安徽 合肥 230601
  • 2. 安徽中医药大学药学院,安徽省中药研究与开发重点实验室,省部共建新安医学教育部重点实验室,安徽 合肥 230038
  • 折叠

摘要

Abstract

Aim To investigate the effects of paeonol on lipopolysaccharide ( LPS) and adenosine 5′-triphos-phate ( ATP) induced NLRP3 inflammasome activation in primary rat microglia and the mechanisms responsi-ble for this anti-inflammatory effects. Methods Pri-mary rat microglia were identified immunohistochemi-cally using the cluster of differentiation 11 b ( CD11 b ) antibody. Proinflammatory cytokine IL-1β was deter-mined by ELISA. Western blot was performed to ob-serve the protein expression of NLRP3 , ASC and caspase-1 in cultured primary rat microglia. The level of intracellular reactive oxygen species ( ROS) was mo-nitored by using the fluorescent probe 2′, 7′-dichlo-rofluorescein diacetate ( DCFH-DA ) . Results LPS (0. 5 mg · L-1 )/ATP ( 5 mmol · L-1 ) significantly increased intracellular ROS level and IL-1β secretion and upregulated NLRP3 , ASC and caspase-1 protein expression in primary rat microglia. Paeonol signifi-cantly decreased intracellular ROS level and IL-1β se-cretion, and inhibited LPS/ATP induced overexpres-sion of NLRP3 , ASC and caspase-1 in cultured primary rat microglia. Conclusion Paeonol can inhibit LPS/ATP induced NLRP3 inflammasome activation in pri-mary rat microglia, and this inhibitory effect may be through the suppression of intracellular ROS.

关键词

丹皮酚/LPS/ATP/小胶质细胞/NLRP3 炎症小体/ROS

Key words

paeonol/LPS/ATP/microglia/NLRP3 in-flammasome/ROS

分类

医药卫生

引用本文复制引用

王伟,戴敏,徐忠东..丹皮酚对脂多糖/三磷酸腺苷诱导的小胶质细胞NLRP3炎症小体激活的影响[J].中国药理学通报,2014,(5):652-656,5.

基金项目

国家自然科学基金资助项目( No 81274134) ( No 81274134)

安徽省自然科学基金资助项目(No 1408085MH146) (No 1408085MH146)

安徽省高校省级自然科学研究项目(No KJ2013Z275,KJ2014A202) (No KJ2013Z275,KJ2014A202)

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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