Cinnamaldehyde protects VSMCs against ox-LDL-induced proliferation and migration through S arrest and inhibition of p38, JNK/MAPKs and NF-κB.

ABSTRACT

Cinnamaldehyde (Cin), as a traditional flavor constituent isolated from the bark of Cinnamonum cassia Presl, has been commonly used for - digestive, cardiovascular and immune system diseases. The pathology of vascular smooth muscle cells (VSMCs) accelerated the progression of atherosclerosis. In our study, we found that cinnamaldehyde significantly suppressed ox-LDL-induced VSMCs proliferation, migration and inflammatory cytokine overproduction, as well as foam cell formation in VSMCs and macrophages. Moreover, cinnamaldehyde inhibited the phosphorylation of p38, JNK and p65 NF-κB and increased heme oxygenase-1 (HO-1) activity. In addition, cinnamaldehyde reduced monocyte chemotactic protein-1 (MCP-1), matrix metalloproteinase-2 (MMP-2) and lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) expression. Furthermore, cinnamaldehyde arrested cell cycle in S phase. Thus, results indicated that cinnamaldehyde antagonized the ox-LDL-induced VSMCs proliferation, migration, inflammation and foam cell formation through regulation of HO-1, MMP-2, LOX-1 and blockage of cell cycle, and - suppression of p38, JNK/MAPK and NF-κB signaling pathways.