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J.M. Waddell, A. Manivannan, M.A. Cotter, J.V. Forrester; Effect of Rosuvastatin on Leukocyte Adhesion in Diabetic Retinopathy . Invest. Ophthalmol. Vis. Sci. 2005;46(13):420.
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Purpose: Previous studies have shown that HMG–CoA reductase inhibitors, collectively known as statins, have immunomodulatory effects independent of their lipid lowering properties. The aim of this study was to investigate the effect of Rosuvastatin, a novel lipid lowering drug, on leukocyte–endothelial interactions in the streptozotocin diabetic mouse model. Methods: Animals were divided into four groups; untreated normal mice, untreated diabetic mice, Rosuvastatin treated normal mice and Rosuvastatin treated diabetic mice. Diabetes duration was 2 weeks. Leukocytes were isolated from spleens of donor mice and labelled with the fluorescent tag calcein–AM. Leukocytes were transferred between various combinations of normal, diabetic and treated mice. Leukocytes were imaged in the retina using a scanning laser ophthalmoscope (SLO) and images were recorded on video tape (S–VHS) for later analysis of leukocyte adhesion to the retinal vessels. Results:Leukocytes from diabetic animals transferred into diabetic mice adhered more readily to the retinal vessels than leukocytes from normal mice transferred into normal mice. This increased leukocyte adherence in diabetic mice was abrogated by Rosuvastatin treatment of both donor and recipient mice. A similar effect was observed when leukocytes from untreated diabetic mice were transferred into Rosuvastatin treated diabetic mice. There was no difference in leukocyte adhesion in treated normal mice compared with untreated normal mice. Conclusions: These results confirm previous reports indicating that leukocyte adhesion is, in part at least, responsible for the capillary occlusions that occur in diabetic retinopathy. Rosuvastatin may be effective in the treatment of diabetic retinopathy by preventing leukocyte adhesion to the vascular endothelium in retinal vessels and it appears to exert its effects at the level of the endothelium. This work is supported by Astra–Zeneca.
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