"treating diseases caused by oxidative stress, such as neuronal hypoxia, by administering a prophylactic or therapeutically effective amount of a cannabinoid to a subject who has a disease caused by oxidative stress.
The cannabinoid may be a cannabinoid other than THC, HU-210, or other potent cannabinoid receptor agonists. The cannabinoid may also be other than HU-211 or any other NMDA receptor antagonist that has previously been reported. A potent cannabinoid receptor agonist is one that has an EC.sub.50 at the cannabinoid receptor of 50 nM or less, but in more particular embodiments 190 nM or 250 nM or less. In disclosed embodiments the cannabinoid is not psychoactive, and is not psychotoxic even at high doses. In some particularly disclosed embodiments, the cannabinoid is selected from the group"
We got here some contradiction, as THC is a cb1 agonist :
AbstractAims. Here we investigated the mechanisms by which cardiovascular CB1 cannabinoid receptors may modulate the cardiac dysfunction, oxidative stress,
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"the endocannabinoids by activating CB1 receptors in cardiomyocytes can trigger increased reactive oxygen species production, MAPK activation, and cell death. Consistent with our results in cardiomyocytes, a recent study has elegantly demonstrated a pivotal role of CB1 receptors in reactive oxygen species generation by macrophages.
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Collectively, these data suggest that CB1 activation in cardiomyocytes amplifies the reactive oxygen/nitrogen species-MAPK activation-cell death pathway in pathological conditions when the endocannabinoid synthetic or metabolic pathways are dysregulated by excessive inflammation and/or oxidative/nitrosative stress (e.g. in various forms of shock, cardiomyopathy/heart failure, and atherosclerosis), which contributes to the pathophysiology of these cardiovascular diseases (as also demonstrated presently in case of DOX-induced cardiomyopathy models). In these diseases,
CB1 receptor antagonists with limited CNS penetration may offer a cardioprotective strategy. Our results also unravel the fundamentals of the CB1 signalling in human cardiomyocytes facilitating the better understanding of the beneficial effects of CB1 antagonists observed in preclinical cardiovascular disease models, as well as in clinical trials. The resistance of CB1 knockout mice against myocardial fibrosis in the chronic cardyomyopathy model may also have very important clinical implications and should be explored in the future studies. Furthermore these CB1-mediated signalling mechanisms may also be involved in cardiotoxicity of cannabis occasionally reported in some users"