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Life Sci. 2013 Mar 21;92(10):582-8. doi: 10.1016/j.lfs.2013.01.021. Epub 2013 Jan 28.

Enhancement of lipopolysaccharide-induced toll-like receptor 2 expression and inflammatory cytokine secretion in HUVECs under high glucose conditions.

Author information

1
Department of Pathology and Pathophysiology, Zhejiang University School of Medicine, Hangzhou 310058, China.

Abstract

AIMS:

Endothelial inflammatory responses mediated by toll-like receptors (TLRs) play an important role in atherogenesis. We aimed to investigate the exacerbation of an inflammatory response in human umbilical vein endothelial cells (HUVECs) under high glucose conditions.

MAIN METHODS:

HUVECs were exposed to normal glucose (5.5 mmol/L) and high glucose (25, 50 mmol/L), alone or with lipopolysaccharide (LPS 0, 10, 100, or 1000 μg/L). Then concentrations of TNF-α and IL-6 in the culture supernatants were determined. The expression of toll-like receptor 2 (TLR2), TLR4 and NF-κB was evaluated by Western blot and RT-PCR analysis.

KEY FINDINGS:

Compared with the normal glucose group, exposure of HUVECs to 50 mmol/L of glucose or 1000 μg/L of LPS significantly increased the concentrations of TNF-α and IL-6 in the culture supernatants. Neither 25 mmol/L of glucose nor low concentration of LPS (≤100 μg/L) alone had an effect on TNF-α and IL-6 release, or TLR2 expression, but they stimulated the inflammatory response and TLR2 expression under high glucose conditions (25 mmol/L) in combination. LPS (100 μg/L) did not alter the TLR4 expression in HUVECs under high glucose condition. Co-incubation with glucose and LPS increased the nuclear NF-κB expression in endothelial cells. Both NF-κB inhibitor and ROS scavenger could inhibit the enhancement of LPS-induced TLR2 expression and inflammatory cytokine secretion under high glucose conditions.

SIGNIFICANCE:

We show in vitro data on the potential role of high glucose in increasing LPS-induced TLR2 expression and inflammatory cytokine secretion in HUVECs, offering a new insight into the pathophysiological pathways involved in atherosclerosis.

PMID:
23369747
DOI:
10.1016/j.lfs.2013.01.021
[Indexed for MEDLINE]

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