期刊
BIOMEDICINE & PHARMACOTHERAPY
卷 95, 期 -, 页码 1777-1788出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2017.09.103
关键词
Cordycepin; Inflammatory cytokines; NOD-Like Receptor Protein 3 inflammasome; ERK
资金
- National Institutes of Health [R01 1R01DK104893, R01DK-057543-11]
- VA Merit Award [I01BX001390]
- National Natural Science Foundation of China [81070245, 81270489, 81320108029, 81274146]
- VCU Massey Cancer Pilot grant [A35362]
- Specific Fund for Public Interest Research of Traditional Chinese Medicine, Ministry of finance [201507004-002]
- National Major Scientific and Technological Special Project for Significant New Drugs Creation project [2015ZX09501004-002-004]
Aim: The aim of this study is to examine the effects of cordycepin (CRD) on LPS-induced inflammatory response in macrophages and further investigate the underlying molecular mechanisms. Methods: Cultured mouse RAW264.7 macrophages and human THP-1-derived macrophages were used in this study. The mRNA and protein expression levels of cytokine IL-1 beta, IL-6, TNF-alpha, and MCP-1 were detected by real time RT-PCR, ELISA and Western blot, respectively. The activation of NOD-Like Receptor Protein 3 (NLRP3) inflammasome was analyzed with Western blot analysis and immunofluorescence staining. The ERK1/2 activation was assessed by Western blot analysis. Results: The results demonstrated that pretreatment with CRD (6.25, 12.5, 25, 50 mu mol/L) dose-dependently inhibited LPS-induced expression of proinflammatory cytokines (IL-1 beta, IL-6, TNF-alpha, MCP-1) and cyclooxygenase 2 (COX-2) in mouse RAW264.7 cells. Similar results were obtained in human THP-1-derived macrophages with CRD. Furthermore, CRD remarkably inhibited LPS-induced activation of the NLRP3 inflammasome and ERK1/2 signaling pathway in RAW264.7 cells. Conclusion: CRD exerts anti-inflammatory effects in LPS-induced murine and human macrophages at least in part by inhibiting the activation of NLRP3 inflammasome and ERK1/2 signaling pathway as well as inhibition of COX2-mediated inflammatory response.
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