Curcumin inhibits the expression of COX-2 in UVB-irradiated human keratinocytes (HaCaT) by inhibiting activation of AP-1: p38 MAP kinase and JNK as potential upstream targets.
- Author:
Jae We CHO
1
;
Kun PARK
;
Gi Ryang KWEON
;
Byeong Churl JANG
;
Won Ki BAEK
;
Min Ho SUH
;
Chang Wook KIM
;
Kyu Suk LEE
;
Seong Il SUH
Author Information
1. Department of Dermatology Keimyung University, School of Medicine 194 DongSan-dong Jung-gu, Daegu 700-712, Korea. seong@dsmc.or.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
COX-2;
curcumin;
HaCaT;
MAPK;
UVB
- MeSH:
Curcumin/*pharmacology;
Enzyme Activation/drug effects/radiation effects;
Enzyme Inhibitors/pharmacology;
Humans;
JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism;
Keratinocytes/cytology/*drug effects/*radiation effects;
Prostaglandin-Endoperoxide Synthase/*metabolism;
Research Support, Non-U.S. Gov't;
Transcription Factor AP-1/*metabolism;
Ultraviolet Rays;
p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism
- From:Experimental & Molecular Medicine
2005;37(3):186-192
- CountryRepublic of Korea
- Language:English
-
Abstract:
Ultraviolet B (UVB) irradiation of skin induces an acute inflammation. Cyclooxygenase-2 (COX-2) protein plays key roles in acute inflammation in UVB-irradiated keratinocyte cell line HaCaT. Recently, curcumin has been regarded as a promising anti-inflammatory agent due to its ability to inhibit COX-2 expression. However, it remains largely unknown whether curcumin inhibits the UVB-induced COX-2 expression in HaCaT cells. This study was undertaken to clarify the effect of curcumin on the expression of COX-2 in UVB- irradiated HaCaT cells and further determined the molecular mechanisms associated with this process. In this study, we have found that the expression of COX-2 mRNA and protein were up-regulated in UVB-irradiated HaCaT cells in a dose- and time-dependent manner. Interestingly, treatment with curcumin strongly inhibited COX-2 mRNA and protein expressions in UVB-irradiated HaCaT cells. Notably, there was effective inhibition by curcumin on UVB-induced activations of p38 MAPK and JNK in HaCaT cells. The DNA binding activity of AP-1 transcription factor was also markedly decreased with curcumin treatment in UVB-irradiated HaCaT cells. These results collectively suggest that curcumin may inhibit COX- 2 expression by suppressing p38 MAPK and JNK activities in UVB-irradiated HaCaT cells. We propose that curcumin may be applied as an effective and novel sunscreen drug for the protection of photoinflammation.
