Abstract:Aim: To investigate the effects of Astragalus polysaccharides (APS) on tumor necrosis factor (TNF)-α-induced inflammatory reactions in human umbilical vein endothelial cells (HUVECs) and to elucidate the underlying mechanisms. Methods: HUVECs were treated with TNF-α for 24 h. The amounts of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were determined with Western blotting. HUVEC viability and apoptosis were detected using cell viability assay and Hoechst staining, r… Show more
“…Several lines of evidence have demonstrated that ROS contribute to ICAM-1 expression induced by different stimuli in various cell types (8,34). In addition, NADPH oxidase is an important enzymatic source for the production of ROS under various pathologic conditions.…”
Section: Involvement Of Nadph Oxidase and Ros Generation In Lps-inducmentioning
Cho RL, Yang CC, Lee IT, Lin CC, Chi PL, Hsiao LD, Yang CM. Lipopolysaccharide induces ICAM-1 expression via a c-Src/ NADPH oxidase/ROS-dependent NF-B pathway in human pulmonary alveolar epithelial cells.
“…Several lines of evidence have demonstrated that ROS contribute to ICAM-1 expression induced by different stimuli in various cell types (8,34). In addition, NADPH oxidase is an important enzymatic source for the production of ROS under various pathologic conditions.…”
Section: Involvement Of Nadph Oxidase and Ros Generation In Lps-inducmentioning
Cho RL, Yang CC, Lee IT, Lin CC, Chi PL, Hsiao LD, Yang CM. Lipopolysaccharide induces ICAM-1 expression via a c-Src/ NADPH oxidase/ROS-dependent NF-B pathway in human pulmonary alveolar epithelial cells.
“…Accumulated evidence demonstrates that monocyte infiltration plays a crucial role in the pathophysiology of coronary artery diseases including atherosclerosis, which can not only initiate and propagate the accumulation of monocyte-derived macrophages but also produce inflammatory mediators that destabilize atherosclerotic plaques (Kartikasari et al, 2009;Zhu et al, 2013). The monocyte-endothelium cells interactions consist of consecutive processes of monocytes adhesion 3 / 29 and infiltration through the endothelium.…”
“…Lauric acid has been shown to reduce the expression of transcription factor, NF-kB [21] . NF-kB is a pro-inflammatory transcription factor that activates immune and inflammatory response by controlling the genes expression of a wide spectrum of inflammatory cytokines and cell adhesion molecules [22][23][24] . Hence, the reduction of IFN-g induced VCAM-1 and ICAM-1 expression might be caused by the diminished cellular NF-kB concentration after the treatment of lauric acid.…”
A B S T R A C TObjective: To investigate the effect of different concentrations of lauric acid on Intercellular Adhesion Molecule-1 (ICAM-1) and Vascular Cell Adhesion Molecule-1 (VCAM-1) expression in IFN-g stimulated human monocytic THP-1 cell line. Methods: THP-1 cell were cultured using Roswell Park Memorial Institute medium supplemented with 10% fetal bovine serum. THP-1 monocytes were firstly differentiated into macrophages by using phorbol-12-myristate-13-acetate. IFN-g response test was performed and total cellular RNA was extracted using TRI Reagent ® LS before q-RT-PCR was carried out. Subsequently, IFN-g treated THP-1 macrophages were stimulated with increasing doses of lauric acid for another 24 h, before q-RT-PCR.Results: The mRNA expression levels of ICAM-1 and VCAM-1 were normalized to bactin and relatived to the untreated cells. The expressions of ICAM-1 and VCAM-1 were significantly induced in cells treated with 10 ng/mL of IFN-g. This showed that IFN-g could up-regulate inflammatory process and may cause atheroma formation. MTT assay was carried out to investigate the effect of lauric acid on undifferentiated and differentiated THP-1 cells. Although lauric acid did not have any significant impact on undifferentiated and differentiated THP-1 cell viability, the normalized fold expressions of ICAM-1 and VCAM-1 in IFN-g-treated THP-1 macrophages were decreased significantly in a dose dependent manner with the presence of increasing doses of lauric acid. Conclusions: This study successfully proved that lauric acid was able to antagonize the up-regulatory effect of IFN-g on ICAM-1 and VCAM-1 expressions in THP-1 macrophages. This indicates that lauric acid may be an anti-inflammatory therapeutic and prophylaxis agent for atherosclerosis.
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