Cinnamaldehyde protects against oxidative stress and inhibits the TNF­α­induced inflammatory response in human umbilical vein endothelial cells.

ABSTRACT

Oxidative stress and inflammation play critical roles in the development of cardiovascular diseases. Cinnamaldehyde (CA) is a natural compound from Cinnamomum cassia, and its anticancer, antimicrobial and anti­inflammatory activities have been widely investigated. In the present study, the cytoprotective and anti­inflammatory effects of CA on H2O2­ or tumor necrosis factor (TNF)­α­exposed human umbilical vein endothelial cells (HUVECs) were examined. CA and its natural derivative, 2­methoxycinnamaldehyde (MCA), markedly increased the cellular protein level of heme oxygenase­1 (HO­1) and promoted the translocation of nuclear factor erythroid 2­related factor 2 (Nrf2) to the nucleus. CA­mediated Nrf2/HO­1 activation protected the HUVECs from H2O2­induced oxidative stress, which promotes apoptosis. HO­1 depletion by siRNA attenuated the CA­mediated cell protective effects against oxidative stress. Additionally, CA markedly inhibited the adhesion of U937 monocytic cells to HUVECs by decreasing the expression level of vascular cell adhesion protein 1 (VCAM­1). An in vivo experiment confirmed the anti­inflammatory effects of CA, as lipopolysaccharide (LPS)­induced inflammatory cell infiltration was effectively inhibited by the compound. Overall, these observations suggest that CA may be used as a therapeutic agent for oxidative stress­mediated cardiovascular diseases, such as atherosclerosis.