Document Detail


Chamomile: an anti-inflammatory agent inhibits inducible nitric oxide synthase expression by blocking RelA/p65 activity.
MedLine Citation:
PMID:  21042790     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Chamomile has long been used in traditional medicine for the treatment of inflammation-related disorders. In this study we investigated the inhibitory effects of chamomile on nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression, and explored its potential anti-inflammatory mechanisms using RAW 264.7 macrophages. Chamomile treatment inhibited LPS-induced NO production and significantly blocked IL-1β, IL-6 and TNFα-induced NO levels in RAW 264.7 macrophages. Chamomile caused reduction in LPS-induced iNOS mRNA and protein expression. In RAW 264.7 macrophages, LPS-induced DNA binding activity of RelA/p65 was significantly inhibited by chamomile, an effect that was mediated through the inhibition of IKKβ, the upstream kinase regulating NF-κB/Rel activity, and degradation of inhibitory factor-κB. These results demonstrate that chamomile inhibits NO production and iNOS gene expression by inhibiting RelA/p65 activation and supports the utilization of chamomile as an effective anti-inflammatory agent.
Authors:
Natarajan Bhaskaran; Sanjeev Shukla; Janmejai K Srivastava; Sanjay Gupta
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  International journal of molecular medicine     Volume:  26     ISSN:  1791-244X     ISO Abbreviation:  Int. J. Mol. Med.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-02     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9810955     Medline TA:  Int J Mol Med     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  935-40     Citation Subset:  IM    
Affiliation:
Department of Urology, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
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Descriptor/Qualifier:
Grant Support
ID/Acronym/Agency:
R01 AT002709/AT/NCCAM NIH HHS; R01 AT002709-05/AT/NCCAM NIH HHS; R01 CA108512/CA/NCI NIH HHS; R01 CA108512-06A1/CA/NCI NIH HHS

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