PubMed, Scopus, Embase, ProQuest and Google Scholar databases were searched to fined interventional studies from the effects of chromium on inflammatory biomarkers such as tumour necrosis factor a (TNF-a), C-reactive protein (CRP), interleukins, monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1) and adipocytokines in hyperglycaemia and diabetes.
In vitro studies demonstrated dapagliflozin-mediated attenuation of tumour necrosis factor α- and hyperglycaemia-induced increases in intercellular adhesion molecule-1, vascular cell adhesion molecule-1, plasminogen activator inhibitor type 1 and NFκB expression.
Egr-1 downstream gene targets, tissue factor (TF) and intercellular adhesion molecule-1 (ICAM-1) expression were increased in hRECs which was reduced by Egr-1 silencing in hyperglycemia.
Hyperglycemia increased the mRNA expression and protein levels of malondialdehyde (MDA), superoxide dismutase (SOD), monocyte chemoattractant protein‑1 (MCP‑1), intercellular adhesion molecule‑1 (ICAM‑1), fibronectin (FN), collagenase type 1 (COL‑1), HMGB1, RAGE and NF‑κB, and the effects could be reversed by dapagliflozin in a concentration‑dependent manner.
Here, we studied the effects of acute hyperglycemia on in vivo intercellular adhesion molecule-1 (ICAM-1) expression, neutrophil recruitment, and brain damage after ischemia/reperfusion in mice and tested whether the natural antioxidant uric acid was protective.Hyperglycemia was induced by i.p. administration of dextrose 45 min before transient occlusion of the middle cerebral artery.
Our data support that endothelial, rather than monocytic/macrophagic, 12/15-LO has a critical role in hyperglycemia-induced ICAM-1 expression, leukocyte adhesion, and subsequent local retinal barrier dysfunction.
Our results showed that long term hyperglycemia in diabetic rats caused the degeneration of neurons and the up-regulation of serum AGEs, and also the up-regulation of RAGE, NF-kappaB p65, VCAM-1 and ICAM-1 in the brain.
The purpose of this study was to evaluate the enhanced effect of hyperglycemia and the attenuating effect of siRNAs on ICAM-1 expression in cultured endothelial cells.
Chronic treatment with AVE3085 did not alter arterial BP or severe hyperglycaemia, but did lead to significantly increased production of eNOS (+95%), cGMP (+128%) and VASP phosphorylation (+65%) as well as to improved vascular function (+36%) associated with reduced production of ICAM-1 (-36%) and VCAM-1 (-58%).
Thus, ICAM-1 expression may share common genetic modulation with traits related to obesity, insulin resistance, and HDL3 cholesterol, but not with hyperglycemia or hypertension per se.