Neuroinflammatory mediators play a crucial role in the pathophysiology of brain ischemia, exerting either deleterious effects on the progression of tis-sue damage or beneficial roles during recovery and repair. Within hours after the ischemic insult, increased levels of cytokines and chemokines enhance the expression of adhesion molecules on cerebral endothelial cells,

An emerging body of evidence supports a key role for the endocannabinoid system in numerous physiological and pathological mechanisms of the cen-tral nervous system. In the recent past, many experimental studies have examined the putative protective or toxic effects of drugs interacting with cannabinoid receptors or have measured the brain levels of endocannabi-noids inin vitro and in vivo models of cerebral ischemia.

Nuclear factor-kappaB (NF-jB) has been proposed to serve a dual func-tion as a regulator of neuron survival in pathological conditions associated with neurodegeneration. NF-jB is a transcription family of factors com-prising five different proteins, namely p50, RelA⁄p65, c-Rel, RelB and p52, which can combine differently to form active dimers in response to external stimuli.

Because clinical trials of pharmacological neuroprotective strategies in stroke have been disappointing, attention has turned to the brain’s own endogenous strategies for neuroprotection. Two endogenous mechanisms have been characterized so far, namely ischemic preconditioning and ische-mic postconditioning.

Stroke is the third leading cause of death in industrialized countries but efficacious stroke treatment is still an unmet need. Preclinical research indi-cates that different molecules afford protection from ischemic neurodegen-eration, but all clinical trials conducted so far have inexorably failed.

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