Atherosclerosis, which manifests as acute coronary syndrome, stroke, and peripheral arterial diseases, is a chronic inflammatory disease of the arterial wall. Prunella vulgaris, a perennial herb with a worldwide distribution, has been used as a traditional medicine in inflammatory disease. Here, we investigated the effects of P. vulgaris ethanol extract on TNF-α-induced inflammatory responses in human aortic smooth muscle cells (HASMCs). We found that P. vulgaris ethanol extract inhibited adhesion of monocyte/macrophage-like THP-1 cells to activated HASMCs. It also decreased expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin and ROS, No production in TNF-α-induced HASMCs and reduced NF-kB activation. Furthermore, P. vulgaris extract suppressed TNF-α-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK). These results demonstrate that P. vulgaris possesses antiinflammatory properties and can regulate TNF-α-induced expression of adhesion molecules by inhibiting the p38 MAPK/ ERK signaling pathway. [BMB Reports 2013; 46(7): 352-357]
Atherosclerosis is a chronic inflammatory disease of the arterial wall. The expression of adhesion molecules in aortic smooth muscle cells facilitates the accumulation of transmigrated leukocytes within the atherosclerotic vascular wall. The stem of Akebia quinata (A. quinata) has previously been used as a crude drug for treating urinary disorders and inflammatory disease in Korea, China and Japan. In the present study, we investigated the effect of an A. quinata ethanol extract (AQEE) on the expression of adhesion molecules and cyclooxygenase-2 (COX‑2) in tumor necrosis factor α (TNF-α)-induced human aortic smooth muscle cells (HASMCs). The results of the present study demonstrated that AQEE attenuated intercellular adhesion molecule 1, E‑selectin and COX‑2 expression in TNF‑α-stimulated HASMCs and inhibited THP-1 cell adhesion to activated HASMCs. Furthermore, AQEE suppressed the TNF‑α induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and reduced nuclear factor κB (NF-κB; p65) nuclear translocation. The present study demonstrated that AQEE possesses anti‑inflammatory properties and regulates TNF-α-induced expression of adhesion molecules by inhibition of the p38 MAPK/NF-κB signaling pathway.
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