Augusta, GA: Administration of the non-psychoactive cannabinoid cannabidiol (CBD) prevents retinal cell death in the diabetic retina, and may one day prevent blindness in diabetic patients, according to preclinical data published in the January issue of the American Journal of Pathology.

Researchers at the Medical College of Virginia, Department of Pharmacology and Toxicology, investigated the protective effects of CBD in streptozotocin-induced diabetic rats after one, two, or four weeks.

"Experimental diabetes induced significant increases in oxidative stress, retinal neuronal cell death, and vascular permeability," investigators wrote.

"CBD treatment significantly reduced oxidative stress, decreased ... vascular endothelial growth, ... and prevented retinal cell death. ... These results demonstrate that CBD treatment reduced neurotoxicity, inflammation, and blood-retinal barrier (BRB) breakdown in diabetic animals."

Diabetic retinopathy, which is characterized by retinal oxygen deprivation and a breakdown of the blood-retinal barrier, affects approximately 16 million Americans and is the leading cause of blindness in working-age adults.

Previous studies have shown CBD to prevent against neurotoxicity associated with stroke, cerebral infarction (localized cell death in the brain), and ethanol-induced brain damage. Clinical trials have also shown CBD to possess anti-tumoral properties - inhibiting the growth of glioma (brain tumor) cells in a dose dependent manner and selectively inducing apoptosis (programmed cell death) in malignant cells.

Neuroprotective and Blood-Retinal Barrier-Preserving Effects of Cannabidiol in Experimental Diabetes

Azza B. El-Remessy^*, Mohamed Al-Shabrawey, Yousuf Khalifa, Nai-Tse Tsai, Ruth B. Caldwell and Gregory I. Liou

the Vascular Biology Center, Cellular Biology and Anatomy, and the Medical College of Georgia; and the Veterans Affairs Medical Center, Augusta, Georgia

Diabetic retinopathy is characterized by blood-retinal barrier (BRB) breakdown and neurotoxicity. These pathologies have been associated with oxidative stress and proinflammatory cytokines, which may operate by activating their downstream target p38 MAP kinase. In the present study, the protective effects of a nonpsychotropic cannabinoid, cannabidiol (CBD), were examined in streptozotocin-induced diabetic rats after 1, 2, or 4 weeks. Retinal cell death was determined by terminal dUTP nick-end labeling assay; BRB function by quantifying extravasation of bovine serum albumin-fluorescein; and oxidative stress by assays for lipid peroxidation, dichlorofluorescein fluorescence, and tyrosine nitration. Experimental diabetes induced significant increases in oxidative stress, retinal neuronal cell death, and vascular permeability. These effects were associated with increased levels of tumor necrosis factor-, vascular endothelial growth factor, and intercellular adhesion molecule-1 and activation of p38 MAP kinase, as assessed by enzyme-linked immunosorbent assay, immunohistochemistry, and/or Western blot. CBD treatment significantly reduced oxidative stress; decreased the levels of tumor necrosis factor-, vascular endothelial growth factor, and intercellular adhesion molecule-1; and prevented retinal cell death and vascular hyperpermeability in the diabetic retina. Consistent with these effects, CBD treatment also significantly inhibited p38 MAP kinase in the diabetic retina. These results demonstrate that CBD treatment reduces neurotoxicity, inflammation, and BRB breakdown in diabetic animals through activities that may involve inhibition of p38 MAP kinase.

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