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Research: SRIVASTAVA and COLLEAGUES,
Listed in Issue 170
Abstract
SRIVASTAVA and COLLEAGUES, Department of Urology, Case Western Reserve University & University Hospitals Case Medical Center, Cleveland, OH 44106, United States 01342 823771 investigated whether chamomile interferes with the COX-2 pathway.
Background
Inducible cyclooxygenase (COX-2) has been implicated in the process of inflammation and carcinogenesis. Chamomile has long been used in traditional medicine for the treatment of inflammatory diseases. In this study the authors aimed to investigate whether chamomile interferes with the COX-2 pathway.
Methodology
Lipopolysaccharide (LPS)-activated RAW 264.7 macrophages were used as an in vitro model for our studies.
Results
Chamomile treatment inhibited the release of LPS-induced prostaglandin E(2) in RAW 264.7 macrophages. This effect was found to be due to inhibition of COX-2 enzyme activity by chamomile. In addition, chamomile caused reduction in LPS-induced COX-2 mRNA and protein expression, without affecting COX-1 expression. The non-steroidal anti-inflammatory drug, sulindac and a specific COX-2 inhibitor, NS398, were shown to act similarly in LPS-activated RAW 264.7 cells. Our data suggest that chamomile works by a mechanism of action similar to that attributed to ! non-steroidal anti-inflammatory drugs.
Conclusion
These findings add a novel aspect to the biological profile of chamomile which might be important for understanding the usefulness of aqueous chamomile extract in the form of tea in preventing inflammation and cancer.
References
Srivastava JK, Pandey M and Gupta S. Chamomile, a novel and selective COX-2 inhibitor with anti-inflammatory activity. Life Sciences. 85 (19-20): 663-9. Nov 4 2009.