| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
From the Kresge Eye Institute, Wayne State University, Detroit, Michigan.
PURPOSE. Diabetic retinopathy is shown to share many similarities with chronic inflammatory disease, and in diabetes, accelerated apoptosis of retinal capillary cells is evident before histopathology can be seen. The purpose of this study was to examine the effect of interleukin (IL)-1ß on capillary cell apoptosis in rat retina and to determine the effect of antioxidants on diabetes-induced changes in retinal IL-1ß.
METHODS. The effect of injection of IL-1ß into the vitreous (5 ng/5 µL) of normal rats on capillary cell apoptosis (detected by terminal transferase dUTP nick-end labeling [TUNEL]) and formation of acellular capillaries was investigated in the trypsin digested retinal microvessels. The levels of IL-1ß were quantified (by ELISA and Western blot) in the retina of rats diabetic for 2 months, and the effect of administration of antioxidants on diabetes-induced changes in retinal IL-1ß was determined.
RESULTS. The number of TUNEL-positive capillary cells in the retinal microvessels obtained from normal rats that received intravitreal injection of IL-1ß was increased by more than threefold and that of acellular capillaries by more than twofold, compared with the microvessels obtained from rats that received an intravitreal injection of PBS (5 µL) or BSA (5 ng/5 µL). IL-1ß also increased the levels of 8-hydroxy-2'-deoxyguanosine (an indicator of oxidative stress) and nitric oxide by more than 40% and activated NF-
B by 35% to 55%. Two months of diabetes in rats increased retinal IL-1ß levels by more than twofold, and antioxidants inhibited such increases.
CONCLUSIONS. IL-1ß, by activation of NF-B and an increase in oxidative stress, plays an important role in the retinal microvascular disease that is characteristic of diabetic retinopathy. Antioxidants inhibit diabetes-induced increases in retinal IL-1ß. These studies offer a possible rationale to test IL-1ß-targeted therapies to inhibit the development of retinopathy in diabetes.
This article has been cited by other articles:
|
|
 |
|
  J. V. Busik, S. Mohr, and M. B. Grant Hyperglycemia-Induced Reactive Oxygen Species Toxicity to Endothelial Cells Is Dependent on Paracrine Mediators Diabetes, July 1, 2008; 57(7): 1952 - 1965. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Devaraj, A. T. Cheung, I. Jialal, S. C. Griffen, D. Nguyen, N. Glaser, and T. Aoki Evidence of Increased Inflammation and Microcirculatory Abnormalities in Patients With Type 1 Diabetes and Their Role in Microvascular Complications Diabetes, November 1, 2007; 56(11): 2790 - 2796. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Zheng, S. J. Howell, D. A. Hatala, K. Huang, and T. S. Kern Salicylate-Based Anti-Inflammatory Drugs Inhibit the Early Lesion of Diabetic Retinopathy Diabetes, February 1, 2007; 56(2): 337 - 345. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Gastinger, R. S. J. Singh, and A. J. Barber Loss of Cholinergic and Dopaminergic Amacrine Cells in Streptozotocin-Diabetic Rat and Ins2Akita-Diabetic Mouse Retinas. Invest. Ophthalmol. Vis. Sci., July 1, 2006; 47(7): 3143 - 3150. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. A. Kowluru, L. Atasi, and Y.-S. Ho Role of mitochondrial superoxide dismutase in the development of diabetic retinopathy. Invest. Ophthalmol. Vis. Sci., April 1, 2006; 47(4): 1594 - 1599. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. Chen, W. J. Esselman, D. B. Jump, and J. V. Busik Anti-inflammatory Effect of Docosahexaenoic Acid on Cytokine-Induced Adhesion Molecule Expression in Human Retinal Vascular Endothelial Cells Invest. Ophthalmol. Vis. Sci., November 1, 2005; 46(11): 4342 - 4347. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
