Gliclazide treatment lowers serum ICAM-1 levels in poorly controlled type 2 diabetic patients

Papanas, N; Tziakas, Dimitrios; Chalikias, Georgios K.; Floros, Dimitrios; Trypsianis, Grigoris; Papadopoulou, Eirini; Kortsaris, A.; Symeonidis, G.; Souliou, Efimia; Maltezos, Efstratios; Hatseras, D.I.

doi:10.1016/s1262-3636(07)70289-6

Cited by 16 publications

(8 citation statements)

References 45 publications

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“…The LFA-1/ICAM-1 interaction is crucial for the ingress of neutrophils into the inflammatory sites [5,6] . Glibenclamide downregulates the expression of ICAM-1 and LFA-1, and through binding to LFA-1 they interfere with ICAM-1-LFA-1 interaction [7,8] . This important mechanism should be borne in mind as the major mechanism for glibenclamide-induced inhibition of neutrophil activity.…”

mentioning

confidence: 99%

ATP-Sensitive Potassium Channel Blockage Attenuates Cisplatin-Induced Renal Damage: A Novel Molecular Mechanism

Namazi¹

2008

Kidney Blood Press Res

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mentioning

confidence: 99%

ATP-Sensitive Potassium Channel Blockage Attenuates Cisplatin-Induced Renal Damage: A Novel Molecular Mechanism

Namazi¹

2008

Kidney Blood Press Res

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“…Studies have shown that the sulfonylurea hypoglycemic agents can ameliorate endothelial dysfunction. Gliclazide, a second-generation sulfonylurea, inhibits high glucose-mediated expression increase of ICAM-1 through inhibition of a Protein kinase C (PKC) pathway [34]. The immunohistochemistry test in our experiment indicates that I 4 significantly decreases the positive expression of ICAM-1 on HUVECs stimulated by high glucose concentrations.…”

Section: Discussionmentioning

confidence: 52%

Antiplatelet aggregation and endothelial protection of I₄, a new synthetic anti-diabetes sulfonylurea compound

2014

Platelets

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I4 is a new synthetic anti-diabetes sulfonylurea compound. The aim of present study was to investigate the preventive effects and primary action mechanisms of I4 on platelet-mediated arterial thrombosis. Platelet aggregation and 5-hydroxytryptamine (5-HT) secretion ex vivo was detected. The time-to-occlusion (TTO), thrombus weight and content of von Willebrand factor (vWF) in rat model of electrical- and ferric chloride-induced vessel occlusion were determined. Meanwhile, a rat model of type 2 diabetes mellitus (T2DM) was established to evaluate the effect of I4 on levels of plasma p-selectin, 6-keto-prostaglandin F1a (6-keto-PGF1a), thromboxane B2 (TXB2), tissue-type plasminogen activator (t-PA) and type-1 plasminogen activator inhibitor (PAI-1). NO synthesis, NOS activity, adhesion of platelet toward endothelial cell and intercellular adhesion molecule-1 (ICAM-1) expression were examined. Results showed that I4 exhibited a higher inhibitory potency than Glimepiride on ADP-induced platelet aggregation and 5-HT release ex vivo. In addition, I4 reduced the thrombus weight and content of vWF and markedly prolonged TTO. Oral administration of I4 (1 ∼ 10 mg/kg) inhibited p-selectin production, elevated the ratio of plasma 6-keto-PGF1a/TXB2 and t-PA/PAI-1 in T2DM rats. Furthermore, I4 significantly improved NO synthesis and NOS activity, lowered adhesion ratio of platelet toward endothelial cells and ICAM-1 expression on HUVECs. These observations suggest that I4 markedly improves platelet-mediated arterial thrombosis by inhibiting platelet activation and release reaction, ameliorating the endothelial dysfunction such as the suppression of vWF production and the reduction of the overexpression of ICAM-1, displayed its potential in alleviating diabetes-associated vascular complications.

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“…In the perspective of finding pharmacological therapies to prevent inflammation and ulceration of OM, we highlight the need to investigate the pleiotropic effect of commercial drugs, specifically among them gliclazide, an antidiabetic drug classified as second generation sulfonylurea, with secondary anti-oxidant and anti-inflammatory effects (Drzewoski and Zurawska-Klis, 2006; Sliwinska et al, 2012). Gliclazide has an inhibitory effect on adhesion molecules, independent of its hypoglycemic effect (Papanas et al, 2006). The increase in cell adhesion molecule (CAM) expression following treatment with irinotecan can directly affect the normal inflammatory response required after an injury, and can also impact on cell kinetics through indirect effects on the subepithelial extracellular matrix (ECM) in mucositis (Al-Dasooqi et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Gliclazide Prevents 5-FU-Induced Oral Mucositis by Reducing Oxidative Stress, Inflammation, and P-Selectin Adhesion Molecules

et al. 2019

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Oral mucositis (OM) is one of the main side effects of the head and neck cancer treatment, particularly radiotherapy and/or chemotherapy. OM is characterized by ulcers, erythema, dysphagia, xerostomia, and increased susceptibility to opportunistic infections. In the perspective of finding pharmacological therapies to prevent inflammation and ulceration of OM, the investigation of the pleiotropic effect of commercial drugs is needed, among them gliclazide, an antidiabetic drug. This study aimed to evaluate the effect of gliclazide in an experimental OM model induced by 5-fluorouracil. Male hamsters were pre-treated with oral gliclazide (1, 5, or 10 mg/kg) for 10 days. Cheek pouch samples were subjected to histopathological and immunohistochemical analysis (COX 2 , iNOS, MMP-2, NFκB P65, GPx) and imunofluorescence (P-selectin). IL-1β and TNF-α levels, Myeloperoxidase activity (MPO) and malondialdehyde (MDA) levels were investigated by ultraviolet-visible spectroscopy analysis. NFκB NLS P50 protein levels were analyzed by western blotting. The group treated with gliclazide at a dose of 10 mg/kg showed presence of erythema, no evidence of erosion, and absence of mucosal ulceration with a score of 1 (1–2) ( p < 0.01). Histopathological data for the group treated with gliclazide 10 mg/kg showed re-epithelialization, discrete mononuclear inflammatory infiltrate and absence of hemorrhage, edema, ulcers and abscesses with a score of 1 (1–1) ( p < 0.01). Treatment with gliclazide 10 mg/kg reduced MPO activity ( p < 0.001), MDA levels ( p < 0.001) and NFκB NLS P50 ( p < 0.05) protein levels, resulting in low immunostaining to Cox-2, iNOS ( p < 0.05), NFκB P65 ( p < 0.05), and negative immunoreaction to MMP-2 ( p < 0.001). However, it appeared that for Gpx1, the staining was restored in the GLI 10-FUT group compared with 5FUT/saline ( p < 0.05). Immunofluorescence revealed decreased levels of P-selectin ( p < 0.001) after treatment with gliclazide 10 mg/kg ( p < 0.05). In summary, gliclazide accelerated mucosal recovery and reduced oxidative stress and inflammation in the 5-FU-induced OM in hamsters.

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Gliclazide treatment lowers serum ICAM-1 levels in poorly controlled type 2 diabetic patients

Cited by 16 publications

References 45 publications

ATP-Sensitive Potassium Channel Blockage Attenuates Cisplatin-Induced Renal Damage: A Novel Molecular Mechanism

ATP-Sensitive Potassium Channel Blockage Attenuates Cisplatin-Induced Renal Damage: A Novel Molecular Mechanism

Antiplatelet aggregation and endothelial protection of I₄, a new synthetic anti-diabetes sulfonylurea compound

Gliclazide Prevents 5-FU-Induced Oral Mucositis by Reducing Oxidative Stress, Inflammation, and P-Selectin Adhesion Molecules

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Gliclazide treatment lowers serum ICAM-1 levels in poorly controlled type 2 diabetic patients

Cited by 16 publications

References 45 publications

ATP-Sensitive Potassium Channel Blockage Attenuates Cisplatin-Induced Renal Damage: A Novel Molecular Mechanism

ATP-Sensitive Potassium Channel Blockage Attenuates Cisplatin-Induced Renal Damage: A Novel Molecular Mechanism

Antiplatelet aggregation and endothelial protection of I4, a new synthetic anti-diabetes sulfonylurea compound

Gliclazide Prevents 5-FU-Induced Oral Mucositis by Reducing Oxidative Stress, Inflammation, and P-Selectin Adhesion Molecules

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Product

Resources

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Antiplatelet aggregation and endothelial protection of I₄, a new synthetic anti-diabetes sulfonylurea compound