brain ischemia/cannabis

Cannabinoids have neuroprotective potentials, and the expression of endocannabinoids as well as cannabinoid receptors is induced after cerebral ischemia. They also induce hypothermia by lowering the hypothalamic set point. We have estimated the significance of such hypothermia in ischemic

OBJECTIVE To investigate the protective effect of paeoniflorin on hippocampal neurons in rats subjected to cerebral ischemia and reperfusion through activating cannabinoid receptor 2 (CBR2). METHODS A total of 144 male SD rats were randomly divided into sham-operation group, cerebral

BACKGROUND It is reported that endogenous cannabinoids can cause vasodilation and bradycardia. They have anti-inflammatory effect and protect endothelial cells from injury, therefore they have potential application prospect in the prevention of cardio-cerebrovascular diseases. However, the

OBJECTIVE To investigate the neuroprotective effect of preconditioning with cannabinoid (CB) receptor agonist WIN 55, 212 - 2 on focal cerebral ischemia. METHODS Fifty male SD rats were randomly assigned to 5 equal groups: control group undergoing middle cerebral artery occlusion (MCAO) for 2 h only

The endocannabinoid system is crucially involved in the regulation of brain activity and inflammation. We have investigated the localization of cannabinoid CB1 and CB2 receptors in adult rat brains before and after focal cerebral ischemia due to endothelin-induced transient occlusion of the middle

Neonatal hypoxic-ischemic encephalopathy (NHIE) is a devastating condition for which effective therapeutic treatments are still unavailable. Cannabinoids emerge as neuroprotective substances in adult animal studies; therefore, we aimed herein to test whether cannabinoids might reduce brain damage

This study was performed to investigate whether WIN 55,212-2 (WIN), a cannabinoid receptor agonist, could attenuate blood-brain barrier (BBB) disruption in focal cerebral ischemia in rats and whether the CB 1 receptor antagonist rimonabant could prevent this attenuation. A total of 0.3 or 1 mg/kg of

We demonstrated in our previous research that pretreatment with electroacupuncture (EA) induces rapid (2h after EA) and delayed (24h after EA) tolerance to focal cerebral ischemia. We further elucidate the endocannabinoid and cannabinoid receptor type 1(CB1) involvment in the rapid ischemic

Marijuana and related drugs (cannabinoids) have been proposed as treatments for a widening spectrum of medical disorders. R(+)-[2, 3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1, 4-benzoxazin-yl]-(1-naphthalenyl)methanone mesylate (R(+)-WIN 55212-2), a synthetic cannabinoid agonist,

One of the most important causes of morbidity and mortality is neurologic dysfunction; its high incidence has led to an intense research of the mechanisms that protect the central nervous system from hypoxia and ischemia. The mayor challenge is to block the biochemical events leading to neuronal

Activation of the cannabinoid 2 receptor (CB(2)) reduces ischemic injury in several organs. However, the mechanisms underlying this protective action are unclear. In a mouse model of ischemic stroke, we show that the CB(2) agonist JWH-133 (1 mg . kg(-1) . d(-1)) decreases the infarct size measured 3

The cerebrovascular effects of marijuana use are not well described. With increasing legalization of cannabis for medical and recreational use in North America, identification of potential risks of the drug is necessary. We present the case of a 31-year-old man who had two ischemic infarctions in

Some occluded arteries of acute ischemic stroke (AIS) patients are not recanalized, even if thrombolytic therapy is performed. Considering such clinical settings, we examined the potential cerebroprotective efficacy of TAK-937, a novel cannabinoid receptor agonist, in young adult and aged rats with

The human costs of stroke are very large and growing; it is the third largest cause of death in the United States and survivors are often faced with loss of ability to function independently. There is a large need for therapeutic approaches that act to protect neurons from the injury produced by