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Träfflista för sökning "WFRF:(Smith Maj Lis) srt2:(2005-2009)"

Sökning: WFRF:(Smith Maj Lis) > (2005-2009)

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1.
  • Agardh, Carl-David, et al. (författare)
  • The Aldose Reductase Inhibitor Fidarestat Suppresses Ischemia-Reperfusion-Induced Inflammatory Response in Rat Retina.
  • 2009
  • Ingår i: Pharmacology. - : S. Karger AG. - 1423-0313 .- 0031-7012. ; 84:5, s. 257-263
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent studies suggest that increased aldose reductase (AR) activity plays an important role in ischemia-reperfusion injury in the retina. The mechanisms are not completely understood, but may be linked to inflammation. In the present study, we investigated whether the AR inhibitor fidarestat suppressed the retinal inflammatory response induced by ischemia-reperfusion in a rat model. The inflammatory response was manifested by increased gene expression of tumor necrosis factor-alpha and intercellular adhesion molecule-1 (ICAM-1) as well as elevated protein levels of soluble ICAM-1. This response was partially suppressed by the AR inhibitor fidarestat. The findings may reveal beneficial effects of AR inhibition on retinal inflammation associated with ischemia-reperfusion and are in agreement with recent developments in pharmacological research suggesting that pathological conditions other than diabetes may benefit from AR inhibitors.
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2.
  • Öhman, Jenny, et al. (författare)
  • Tumor necrosis factor-alpha does not mediate diabetes-induced vascular inflammation in mice.
  • 2009
  • Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - 1524-4636 .- 1079-5642. ; 29:10, s. 1465-1470
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Vascular inflammation is a key feature of both micro- and macrovascular complications in diabetes. Several lines of evidence have implicated the cytokine tumor necrosis factor (TNF) alpha as an important mediator of inflammation in diabetes. In the present study we evaluated the role of TNF alpha in streptozotocin (STZ)-induced diabetes on vascular inflammation in C57BL/6 wild-type and apoE-/- mice. METHODS AND RESULTS: Diabetes increased the expression of vascular cell adhesion molecule (VCAM)-1 in cerebral arteries 150 m in diameter as well as the macrophage accumulation in aortic root atherosclerotic plaques in apoE-/- mice. A more pronounced vascular inflammatory response was observed in diabetic TNF alpha-deficient apoE-/- mice. These mice were also characterized by increased accumulation of IgG and IgM autoantibodies in atherosclerotic lesions. Diabetes also increased VCAM-1 expression and plaque formation in apoE-competent TNF alpha -/- mice, whereas no such effects were observed in C57BL/6 wild-type mice. CONCLUSIONS: The present findings suggest that TNF alpha does not mediate diabetic-induced vascular inflammation in mice and reveal an unexpected protective role for TNF alpha. These effects are partly attributable to a direct antiinflammatory role of TNF alpha, but may also reflect a defective development of the immune system in these mice.
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