Effect of Zanthoxylum schinifolium on TNF-α-induced vascular inflammation in human umbilical vein endothelial cells |
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Authors: | Li Hua Cao Yun Jung Lee Dae Gill Kang Jin Sook Kim Ho Sub Lee |
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Affiliation: | aProfessional Graduate School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk, 570-749, Republic of Korea;bMedical Resources Research Institute (MeRRI), Wonkwang University, Iksan, Jeonbuk, 570-749, Republic of Korea;cKorea Institute of Oriental Medicine, Jeonmin-dong, Yusung-gu, Daejeon, 305-811, Republic of Korea |
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Abstract: | Pro-inflammatory cytokines induce the injury of endothelial cells in response to increases of adhesion molecules, leading to vascular inflammation and the development of atherosclerosis. In this study, we evaluated an ethanol extract of Zanthoxylum schinifolium (EZS) to determine if it inhibits the expressions of cellular adhesion molecules in human umbilical vein endothelial cells (HUVEC). When pretreatment of HUVEC with EZS, EZS suppressed the expression levels of cell adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin induced by TNF-α. The adhesion of HL-60 cells to TNF-α-induced endothelial cells was decreased significantly in a concentration-dependent manner. Furthermore, TNF-α-induced MCP-1 and IL-8 mRNA expression levels were also attenuated by pretreatment with EZS. In addition, EZS suppressed TNF-α-induced production of reactive oxygen species (ROS). EZS inhibited NF-κB activation and IκB-α phosphorylation induced by TNF-α, subsequent degradation of IκB-α. Finally, EZS inhibited TNF-α-induced p38 MAPK and c-Jun N-terminal kinase (JNK) phosphorylation. Taken together, these results demonstrate that EZS suppresses vascular inflammatory process, which may be closely related to the inhibition of ROS, JNK, p38 MAPK and NF-κB activation in HUVEC. |
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Keywords: | Zanthoxylum schinifolium ROS Cell adhesion molecules Vascular inflammation NF-κ B HUVEC |
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