RT Journal Article
ID 02d42a8c0d78af0a
A1 Lee, Yong Soo
A1 Kwon, Eun Jin
A1 Jin, Da Qing
A1 Park, Seung Hee
A1 Kang, Young Shin
A1 Huh, Keun
A1 Kim, Jung-Ae
T1 Redox Status-Dependent Regulation of Cyclooxygenases Mediates the Capsaicin-Induced Apoptosis in Human Neuroblastoma Cells
JF Journal of Environmental Pathology, Toxicology and Oncology
JO JEP(T)
YR 2002
FD 2002-06-01
VO 21
IS 2
OP 8
AB 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.
PB Begell House
LK https://www.dl.begellhouse.com/journals/0ff459a57a4c08d0,4ac6c8531cba5202,02d42a8c0d78af0a.html