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 anti-inflammatory activities have been widely investigated. In the present study, the cytoprotective and anti-inflammatory effects of CA on H2O2- or tumor necrosis factor (TNF)-α-exposed human umbilical vein endothelial cells (HUVECs) were examined. CA and its natural derivative, 2-methoxycinnamaldehyde (MCA), markedly increased the cellular protein level of heme oxygenase-1 (HO-1) and promoted the translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) to the nucleus. CA-mediated Nrf2/HO-1 activation protected the HUVECs from H2O2-induced oxidative stress, which promotes apoptosis. HO-1 depletion by siRNA attenuated the CA-mediated 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 (VCAM-1). An in vivo experiment confirmed the anti-inflammatory effects of CA, as lipopoly-saccharide (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 stress-mediated cardiovascular diseases, such as atherosclerosis.
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