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ISSN Druckformat: 0731-8898
ISSN Online: 2162-6537
IF:
2.4
5-Year IF:
2.8
Immediacy Index:
0.5
Eigenfactor:
0.00049
JCI:
0.59
SJR:
0.429
SNIP:
0.507
CiteScore™::
3.9
H-Index:
49
Indexed in
Redox Status-Dependent Regulation of Cyclooxygenases Mediates the Capsaicin-Induced Apoptosis in Human Neuroblastoma Cells
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ABSTRAKT
Cyclooxygenases (COX) appear to be involved in the mechanism of apoptosis in various cancer cells. In this study we investigated the role of COX in the capsaicin (Cap)-induced apoptosis in SK-N-SH human neuroblastoma cells. Cap induced decreased cell viability and apoptosis in a dose-dependent manner. Cap also significantly reduced the basal generation of reactive oxygen species (ROS) and lipid peroxidation in a time-dependent fashion. Cap markedly suppressed the expression of COX-1 and COX-2. Pretreatment with NS-398, a selective COX-2 inhibitor, or indomethacin, a nonselective COX inhibitor, significantly enhanced the Cap-induced decreased cell viability and apoptosis. Exogenous application of an oxidant, Н2О2, significantly prevented the Cap-induced apoptosis and suppressed the expression of COX isoforms. These results suggest that redox status-dependent regulation of COX expression may mediate apoptosis induced by Cap in human neuroblastoma cells.
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