Rosiglitazone influences the expression of leukocyte adhesion molecules and CD14 receptor in type 2 diabetes mellitus patients
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
24908235
DOI
10.33549/physiolres.932791
PII: 932791
Knihovny.cz E-zdroje
- MeSH
- biologické markery krev MeSH
- diabetes mellitus 2. typu krev farmakoterapie imunologie MeSH
- down regulace MeSH
- hypoglykemika terapeutické užití MeSH
- krevní glukóza účinky léků metabolismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- lipopolysacharidové receptory krev MeSH
- mediátory zánětu krev MeSH
- molekuly buněčné adheze krev MeSH
- rosiglitazon MeSH
- senioři MeSH
- studie případů a kontrol MeSH
- thiazolidindiony terapeutické užití MeSH
- výsledek terapie MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- biologické markery MeSH
- hypoglykemika MeSH
- krevní glukóza MeSH
- lipopolysacharidové receptory MeSH
- mediátory zánětu MeSH
- molekuly buněčné adheze MeSH
- rosiglitazon MeSH
- thiazolidindiony MeSH
Diabetes mellitus is associated with increased inflammatory response, which may contribute to atherosclerosis progression. Experimental results demonstrated anti-inflammatory activity of glitazones; their effect on leukocyte adhesion molecules has not been studied to date. We therefore studied the effect of rosiglitazone treatment on leukocyte surface expression of adhesion molecules in patients with type 2 diabetes mellitus and compared our results with findings in healthy subjects. 33 subjects with type 2 diabetes and 32 healthy controls were included; patients were examined at baseline and after 5 months of rosiglitazone treatment (4 mg/d). Leukocyte expression of adhesion molecules LFA-1, CD18 and ICAM-1 was quantified using flow cytometry; in addition, CD14 (lipopolysaccharide receptor) expression was analyzed as a marker of nonspecific immunity. The expression of examined molecules at baseline was higher in patients compared to controls. Despite only mild decrease in blood glucose, rosiglitazone treatment induced substantial decrease of CD18 and CD14 expression and borderline decrease of LFA-1 and ICAM-1 expression (on monocytes only). We thus observed improvement in the expression of leukocyte inflammatory markers after rosiglitazone treatment. This effect is supposed to be mediated by direct effect of rosiglitazone on PPAR-gamma receptors on leukocytes.
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