Capsaicin inhibits platelet-activating factor-induced cytosolic Ca2+ rise and superoxide production
SCIE
SCOPUS
- Title
- Capsaicin inhibits platelet-activating factor-induced cytosolic Ca2+ rise and superoxide production
- Authors
- Choi, SY; Ha, H; Kim, KT
- Date Issued
- 2000-10-01
- Publisher
- AMER ASSOC IMMUNOLOGISTS
- Abstract
- 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.
- Keywords
- MEDIATED CALCIUM-ENTRY; PROTEIN-KINASE-A; HL-60 CELLS; HUMAN NEUTROPHILS; SUBSTANCE-P; GRANULOCYTIC DIFFERENTIATION; PHOSPHOINOSITIDE HYDROLYSIS; RECEPTOR ANTAGONIST; RESPIRATORY BURST; GANGLION NEURONS
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/19852
- DOI
- 10.4049/jimmunol.165.7.3992
- ISSN
- 0022-1767
- Article Type
- Article
- Citation
- JOURNAL OF IMMUNOLOGY, vol. 165, no. 7, page. 3992 - 3998, 2000-10-01
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