Cinnamaldehyde protects against oxidative stress and inhibits the TNF‑α‑induced inflammatory response in human umbilical vein endothelial cells
- Nam‑Yi Kim
- Nguyet‑Tran Trinh
- Sang‑Gun Ahn
- Soo‑A Kim
Affiliations: Department of Biochemistry, Dongguk University College of Oriental Medicine, Gyeongju, North Gyeongsang 38066, Republic of Korea, Department of Pathology, Chosun University College of Dentistry, Gwangju 61452, Republic of Korea
- Published online on: April 16, 2020 https://doi.org/10.3892/ijmm.2020.4582
Copyright: © Kim
et al. This is an open access article distributed under the
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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 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 stress‑mediated cardiovascular diseases, such as atherosclerosis.