These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Effect of Zanthoxylum schinifolium on TNF-alpha-induced vascular inflammation in human umbilical vein endothelial cells.
    Author: Cao LH, Lee YJ, Kang DG, Kim JS, Lee HS.
    Journal: Vascul Pharmacol; 2009; 50(5-6):200-7. PubMed ID: 19563733.
    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-), and E-selectin induced by TNF-alpha. The adhesion of HL-60 cells to TNF-alpha-induced endothelial cells was decreased significantly in a concentration-dependent manner. Furthermore, TNF-alpha-induced MCP-1 and IL-8 mRNA expression levels were also attenuated by pretreatment with EZS. In addition, EZS suppressed TNF-alpha-induced production of reactive oxygen species (ROS). EZS inhibited NF-kappaB activation and IkappaB-alpha phosphorylation induced by TNF-alpha, subsequent degradation of IkappaB-alpha. Finally, EZS inhibited TNF-alpha-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-kappaB activation in HUVEC.
    [Abstract] [Full Text] [Related] [New Search]