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Capsaicin Inhibits Platelet-Activating Factor-Induced Cytosolic Ca²⁺ Rise and Superoxide Production¹

Se-Young Choi^*, Hyunjung Ha and Kyong-Tai Kim^2,*

^* Department of Life Science, Pohang University of Science and Technology, Pohang, Republic of Korea; and Division of Life Sciences, Chungbuk National University, Cheongju, Republic of Korea

Platelet-activating factor (PAF) is an important participant in the inflammatory process. We studied the regulation of PAF activity by capsaicin in human promyelocytic leukemia HL-60 cells. Capsaicin inhibited PAF-induced superoxide production in a concentration-dependent manner. In addition to PAF, the fMLP- and extracellular ATP-induced superoxide productions were inhibited by capsaicin, whereas PMA-induced superoxide production was not affected. In the PAF-stimulated cytosolic Ca²⁺ increase, capsaicin inhibited in particular the sustained portion of the raised Ca²⁺ level without attenuation of the peak height. In the absence of extracellular Ca²⁺, the PAF-induced Ca²⁺ elevation was not inhibited by capsaicin because capsaicin only inhibited the Ca²⁺ influx from the extracellular space. In addition, capsaicin did not affect PAF-induced inositol 1,4,5-trisphosphate production, suggesting that phospholipase C activation by PAF is not affected by capsaicin. Store-operated Ca²⁺ entry (SOCE) induced by thapsigargin was inhibited by capsaicin in a concentration-dependent manner. This capsaicin effect was also observed on thapsigargin-induced Ba²⁺ and Mn²⁺ influx. Furthermore, capsaicin’s inhibitory effect on the thapsigargin-induced Ca²⁺ rise overlapped with that of SK&F96365, an inhibitor of SOCE. Both capsaicin and SK&F96365 also inhibited PAF-induced cytosolic superoxide generation in HL-60 cells differentiated by all-trans-retinoic acid. Our data suggest that capsaicin exerts its anti-inflammatory effect by inhibiting SOCE elicited via PLC activation, which occurs upon PAF activation and results in the subsequent superoxide production.

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