科研之友
微信
新浪微博
Facebook
分享链接
摘要
The activation of endothelial cells (ECs) and migration of vascular smooth muscle cells (VSMCs) have played a crucial role in monocyte chemotaxis/adhesion and intima thickening during vascular injury and atherosclerosis, respectively. Several phenanthrenes isolated from plants and natural products have been shown to possess different bioactivities such as anti-platelet aggregation and anti-inflammation. The current study was designated to investigate the effects of a phenanthrene derivative, 5,7-dimethoxy-1,4-phenanthrenequinone (DMPQ), on cell adhesion molecule (CAM) expression in vascular ECs and migration in VSMCs. The DMPQ attenuated monocyte-EC interaction but it did not affect monocyte adhesion to matrix. In parallel, DMPQ reduced tumor necrosis factor-alpha (TNF-alpha)-induced intercellular adhesion molecule and vascular CAM expression in ECs. DMPQ compromised TNF-alpha-induced I.B activation, nuclear factor-kappa B (NF-kappa B) translocation, and NF-kappa B-DNA complex formation. Moreover, it affected TNF-alpha-and hydrogen peroxide (H2O2)-induced reactive oxygen species production and I kappa B activation. These suggest that DMPQ affects CAM expression by affecting NF-kappa B signaling. Meanwhile, DMPQ could also inhibit platelet-derived growth factor (PDGF)-induced VSMC migration toward collagen by affecting cellular PDGF signaling, including PDGFR beta, PLC gamma, ERK1/2, and Akt phosphorylation. The VSMC adhesion to collagen and collagen-induced focal adhesion kinase activation during cell adhesion were impaired by DMPQ treatment. This study reveals a phenanthrene derivative-DMPQ-with anti-inflammatory and anti-migratory bioactivity toward vascular ECs and SMCs, suggesting its protective effect on vascular injuries.
- 出版日期2017
- 单位长春大学
