Post-ischemic treatment with cannabidiol prevents electroencephalographic flattening, hyperlocomotion and neuronal injury in gerbils

Braida, Daniela; Pegorini, Simona; Arcidiacono, Maria Vittoria; Consalez, G. Giacomo; Croci, Laura; Sala, Mariaelvina

doi:10.1016/s0304-3940(03)00569-x

Cited by 67 publications

(61 citation statements)

References 18 publications

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“…Histological examination showed the complete survival of CA1 neurons in CBD-treated gerbils. 91 A similar effect has been reported by another research group in mice, after middle cerebral artery occlusion; the neuroprotective action of CBD being unaffected by CB 1 receptor blockade. 92 The same research group has verified that this effect was inhibited by WAY100135, a serotonin 5-hydroxytriptamine 1A (5-HT 1A ) receptor antagonist, but not by capsazepine, a vanilloid receptor antagonist, suggesting that the neuroprotective effect of CBD may be due to the increase in cerebral blood flow mediated by the serotonergic 5-HT 1A receptor.…”

Section: Action On Ischemiasupporting

confidence: 73%

Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action

Zuardi

2008

Rev. Bras. Psiquiatr.

356

302

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Section: Action On Ischemiasupporting

confidence: 73%

Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action

Zuardi

2008

Rev. Bras. Psiquiatr.

356

302

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“…(−)-Δ9-tetrahydrocannabinol (THC) and (−)-cannabidiol (CBD) are the marijuana-derived cannabinoids which possess antioxidative and immunosuppressive effects [136]. It has already been established that nonpsychotropic CBD causes a decrease in interleukin-1, TNF-, and interferon-in murine collagen-induced arthritis and prevents central nervous system neuronal damage in gerbils [137]. El-Remessy et al demonstrated the neuroprotective role of both THC and CBD through antioxidant action in NMDA-induced retinal neurotoxicity in rats [138].…”

Section: Cannabidiol As An Emerging and Novel Therapeuticmentioning

confidence: 99%

Molecular mechanisms of Diabetic Retinopathy, general preventive strategies and novel therapeutic targets

Safi¹,

Qvist²,

Kumar³

et al. 2013

Exp Clin Endocrinol Diabetes

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The growing number of people with diabetes worldwide suggests that diabetic retinopathy (DR) and diabetic macular edema (DME) will continue to be sight threatening factors. The pathogenesis of diabetic retinopathy is a widespread cause of visual impairment in the world and a range of hyperglycemia-linked pathways have been implicated in the initiation and progression of this condition. Despite understanding the polyol pathway flux, activation of protein kinase C (KPC) isoforms, increased hexosamine pathway flux, and increased advanced glycation end-product (AGE) formation, pathogenic mechanisms underlying diabetes induced vision loss are not fully understood. The purpose of this paper is to review molecular mechanisms that regulate cell survival and apoptosis of retinal cells and discuss new and exciting therapeutic targets with comparison to the old and inefficient preventive strategies. This review highlights the recent advancements in understanding hyperglycemia-induced biochemical and molecular alterations, systemic metabolic factors, and aberrant activation of signaling cascades that ultimately lead to activation of a number of transcription factors causing functional and structural damage to retinal cells. It also reviews the established interventions and emerging molecular targets to avert diabetic retinopathy and its associated risk factors.

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“…CBD dose was selected based on previous studies showing maximum protection of CBD at the level of 5 mg/kg/day. 26,27 In the current study, CBD was injected 10 mg/kg every 2 days to decrease the frequency of injection. CBD was obtained from National Institute of Drug Abuse (Research Triangle Park, NC), and a fresh solution in 0.25 ml of 1:1:18 of alcohol:cremorphol:Ringer solution was prepared.…”

Section: Animal Preparationmentioning

confidence: 99%

“…The nonpsychotropic CBD has been shown to decrease interleukin-1, TNF-␣, and interferon-␥ in murine collagen-induced arthritis 26 and to prevent central nervous system neuronal damage in gerbils caused by cerebral ischemia. 27 We have recently demonstrated the neuroprotective effect of both THC and CBD via antioxidant action in NMDAinduced retinal neurotoxicity in rats. 28 We have also demonstrated the BRB-preserving effects of blocking oxidative stress in diabetic rats.…”

mentioning

confidence: 98%

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

El-Remessy

Al‐Shabrawey

Khalifa

et al. 2006

The American Journal of Pathology

236

168

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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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Post-ischemic treatment with cannabidiol prevents electroencephalographic flattening, hyperlocomotion and neuronal injury in gerbils

Cited by 67 publications

References 18 publications

Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action

Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action

Molecular mechanisms of Diabetic Retinopathy, general preventive strategies and novel therapeutic targets

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

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