Journal
FRONTIERS IN PHARMACOLOGY
Volume 10, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2019.00178
Keywords
1,8-cineole; human umbilical vein endothelial cell; lipopolysaccharide; NF-kappa B; PPAR-gamma
Categories
Funding
- National Natural Science Foundation of China [81760725, 81360650]
- Modern Novel Drug Project of Guiyang City [20151001-07]
- Fund of High Level Innovation Talents [2015-4029]
- Fund of Innovation Team of Guizhou Province [2015-4025]
- Fund of Innovated Team of the Education Department of Guizhou Province [2014-31]
- Base of International Scientific and Technological Cooperation of Guizhou Province [2017-5802]
- Foundation for Training Programs of Innovation and Entrepreneurship for Undergraduates of National [201710660003]
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1,8-Cineole (eucalyptol), a monoterpene, has been widely reported for the anti-inflammatory effects. Our previous data confirmed that 1,8-cineole ameliorated the inflammatory phenotype of human umbilical vein endothelial cells (HUVECs) by mediating NF-kappa B expression in vitro. At present, we investigated the protection effects of 1,8-cineole on vascular endothelium in lipopolysaccharide (LPS)-induced acute inflammatory injury mice and the potential mechanisms involved in the protection in HUVECs. Results from enzyme linked immunosorbent assays revealed that 1,8-cineole suppressed the secretion of interleukin (IL)-6 and IL-8 and increased the expression of IL-10 in the serum of LPS-induced mice. 1,8-Cineole reduced the inflammatory infiltration and the expression of vascular cell adhesion molecular 1 (VCAM-1) in the sections of thoracic aorta in LPS-induced acute inflammatory mice. Western blotting indicated that 1,8-cineole significantly decreased the phosphorylation of NF-kappa B p65 and increased the expression of PPAR-gamma in the thoracic aorta tissue. 1,8-Cineole increased the expression of PPAR-gamma in LPS-induced HUVECs. 1,8-Cineole and rosiglitazone reduced the protein and mRNA levels of VCAM-1, E-selectin, IL-6, and IL-8 in LPS-induced HUVECs, which could be reversed by the action of GW9662 (inhibitor of PPAR-gamma). 1,8-Cineole and rosiglitazone blocked the LPS-induced I kappa B alpha degradation and NF-kappa B p65 nucleus translocation, which could be reversed by the pretreatment of GW9662 or silence of PPAR-gamma gene. In conclusion, 1,8-cineole attenuated LPS-induced vascular endothelial cells injury via PPAR-gamma dependent modulation of NF-kappa B.
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