Curcumin Attenuates Acrolein-induced COX-2 Expression and Prostaglandin Production in Human Umbilical Vein Endothelial Cells
10.12997/jla.2020.9.1.184
- Author:
Seung Eun LEE
1
;
Hye Rim PARK
;
Seeun JEON
;
Dongkyo HAN
;
Yong Seek PARK
Author Information
1. Department of Microbiology, College of Medicine, Kyung Hee University, Seoul, Korea. yongseek@khu.ac.kr
- Publication Type:Original Article
- From:Journal of Lipid and Atherosclerosis
2020;9(1):184-194
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE:Inflammation is crucial to limiting vascular disease. Previously we reported that acrolein, a known toxin in tobacco smoke, might play an important role in the progression of atherosclerosis via an inflammatory response involving cyclooxygenase-2 (COX-2) and prostaglandin production in human umbilical vein endothelial cells (HUVECs). Curcumin has been known to improve vascular function and have anti-inflammatory properties. In this study, we investigated whether curcumin prevents the induction of inflammatory response caused by acrolein.
METHODS:Anti-inflammatory effects of curcumin were examined in acrolein-stimulated HUVECs. Induction of proteins, mRNA, prostaglandin and reactive oxygen species (ROS) were measured using immunoblot analysis, real-time reverse-transcription polymerase chain reaction, enzyme-linked immunosorbent assay and flow cytometry, respectively.
RESULTS:Curcumin attenuates inflammatory response via inhibition of COX-2 expression and prostaglandin production in acrolein-induced human endothelial cells. This inhibition by curcumin results in the abolition of phosphorylation of protein kinase C, p38 mitogen-activated protein kinase, and cAMP response element-binding protein. Furthermore, curcumin suppresses the production of ROS and endoplasmic reticulum stress via phosphorylation of eukaryotic initiation factor-2α caused by acrolein.
CONCLUSION:These results suggest that curcumin might be a useful agent against endothelial dysfunction caused by acrolein-induced inflammatory response.