Cannabinoid Trans-Caryophyllene Protects Brain Cells From IschemiaMain Category: Stroke
Article Date: 24 Feb 2013
The activation of cortical type 2 cannabinoid (CB2) receptors with cannabinoid trans-caryophyllene (TC) is effectively able to facilitate recovery among ischemic brain injury patients, according to a recent study published in The American Journal of Pathology.
TC is derived from the essential oils of the Cannabis sativa plant, but its structure is very different to other classical cannabinoids - it is not associated with any psychoactive side effects.
Researchers conducted tests in both in vivo and in vitro animal models and found that TC is successfully able to protect brain cells from ischemia.
Brain ischemia occurs when there is a lack of blood flow to the brain, this can sometimes lead to irreversible damage in the form of vascular dementia. It can be quite deadly, according to researchers from the University of California - Los Angeles, around 62% of ischemic stroke patients are re-hospitalized within 12 months and 15% die within a month of being hospitalized.
In cell cultures consisting of oxygen deprived rat cortical neurons and glia, TC reduced neuronal injury and mitochondrial depolarization.
The lead author of the study, Won-Ki Kim, PhD, of the Department of Neuroscience, College of Medicine, Korea University in Seoul, said:
"To our knowledge, novel data presented in this study provide evidence for the first time supporting a previously unappreciated role of cortical CB2R, especially neuronal CB2Rs, in ischemia. This study suggests that further investigation is warranted to establish the clinical usefulness of TC as a preventative and therapeutic agent for treatment of stroke."
The study is the first of its kind to show how CB2R is able to promote neuroprotection. The scientists obstructed the blood flow of the right middle cerebral artery in rats - mimicking the effects of ischemic stroke - and observed whether treating them with TC (three hours following the occlusion) would have any therapeutic effects, some of the rats also received AM630 - a CB2R antagonist.
The results were very promising and blood flow returned to normal within 24 hours among those that solely received TC treatment.
A day following the stroke, the scientists removed the brains of the rats and measured the volume of the infarct and extent of cerebral edema.
In the cortex of both the control and ischemic brains, the authors found evidence of CB2Rs. The finding finally brings to light the fact that CB2Rs are indeed present in the cortex of the brain - something that's been inconclusive for some time.
On its own TC reduced edema by 51.9% as well as lowering infarct size by 53.8%, it was also able to help decrease neuronal injury and intracellular oxidative stress. However, when TC was given along with AM630, the CB2R antagonist was found to disable the neuroprotective effects of TC.
TC is able to promote cAMP responsive element-binding protein (CREB) phosphorylation as well as to increase the expression of brain-derived neurotrophic factor (BDNF) in ischemic tissue.
The results of this study are ground-breaking and show the therapeutic properties of TC in treating ischemic brain injury. More research is still necessary though, the authors stress.
Written by Joseph Nordqvist
Copyright: MediLexicon International Ltd
Original article posted on Medical News Today.
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