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Journal of Environmental Pathology, Toxicology and Oncology
Fator do impacto: 1.625 FI de cinco anos: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN Imprimir: 0731-8898
ISSN On-line: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v21.i2.40
8 pages

Redox Status-Dependent Regulation of Cyclooxygenases Mediates the Capsaicin-Induced Apoptosis in Human Neuroblastoma Cells

Yong Soo Lee
Department of Physiology, College of Medicine, Kwan-dong University, Kangnung, Korea
Eun Jin Kwon
College of Pharmacy, Yeungnam University, Kyongsan, Korea
Da Qing Jin
College of Pharmacy, Yeungnam University, Kyongsan, Korea
Seung Hee Park
College of Pharmacy, Yeungnam University, Kyongsan, Korea
Young Shin Kang
Department of Physiology, College of Medicine, Kwan-dong University, Kangnung, Korea
Keun Huh
College of Pharmacy, Yeungnam University, Kyongsan, Korea
Jung-Ae Kim
College of Pharmacy, Yeungnam University, Dae-Dong 214-1, Kyongsan 712-749, Korea

RESUMO

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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