Abstract
The mechanism of inhibition of Ca 2+ - triggered phospholipase A 2 (PLA 2) activity and respiratory burst in macrophages by capsaicin is assessed. In the present study, it has been shown that capsaicin inhibits calcium-ionophore stimulated pro-inflammatory responses in macrophages such as generation of superoxide anion, PLA 2 activity (IC 50 = 20uM) and membrane lipid peroxidation (IC 50 = 10 uM). Both capsaicin and PLA 2 antagonists altered the kinetics of respiratory burst in a time and dose dependent manner. Arachidonic acid, linoleic acid and SDS restored capsaicin inhibited respiratory burst. Capsaicin and known PLA 2 inhibitors, dexamethasone and indomethacin, inhibited Ca 2+-dependent PLA 2 activity in vitro from macrophages. Inhibition of PLA 2 activity by capsaicin is independent of Ca 2+ and substrate concentration. Fluorescence studies suggest that capsaicin interacts directly with partially purified macrophage PLA 2. Finally, the antioxidant property of capsaicin was comparable to that of butylated hydroxy toludine (BHT). Taken together these results show that capsaicin an antiinflammatory agent with potential clinical application.
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