ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2012
Anti-inflammatory effects of kaempferol-3-O-sophoroside in human endothelial cells.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 60 citations in OpenAlex.
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKaempferol-3-O-sophoroside (KPOS) was isolated from the leaves of cultivated mountain ginseng. Kaempferol (KP) has antitumor, anti-oxidative, anti-allergic and antidiabetic activities but the barrier protective effects and underlying mechanism are not fully identified. In this study, we attempted to determine whether pretreatment with KPOS induced significant barrier protective activities in lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs).
methodsThe anti-inflammatory activities of KPOS were determined by measuring solute flux, neutrophil adhesion and migration and activation of pro-inflammatory proteins in LPS-activated HUVECs.
resultsWe found that KPOS inhibited LPS-induced barrier disruption, expression of cell adhesion molecules, neutrophil adhesion and transendothelial migration of neutrophils to HUVECs. Further studies revealed that KPOS suppressed the production of tumor necrosis factor-α (TNF-α) and activation of nuclear factor-κB (NF-κB) by LPS, and that anti-inflammatory activities of KPOS were better than those of KP.
conclusionCollectively, these results suggest that KPOS possesses barrier integrity activity, inhibitory activity on cell adhesion and migration to endothelial cells by blocking the activation of NF-κB expression and production of TNF-α, thereby endorsing its usefulness as therapy for vascular inflammatory diseases.
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