Endocannabinoids mediate neuroprotection after transient focal cerebral ischemia

@article{Schomacher2008EndocannabinoidsMN,
  title={Endocannabinoids mediate neuroprotection after transient focal cerebral ischemia},
  author={Markus Schomacher and Harald D. M{\"u}ller and Clemens J. Sommer and Stefan Schwab and Wolf R{\"u}diger Sch{\"a}bitz},
  journal={Brain Research},
  year={2008},
  volume={1240},
  pages={213-220}
}
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62 Citations
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62 Citations

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TLDR
The results support the evidence that BCP may be used as a dietary supplement to control the physiological response to the hypoperfusion/reperfusion-induced oxidative stress, and modulates in a beneficial way the ECS activation and the lipoperoxidation, taken as indicative of oxidative stress.
Involvement of the endocannabinoid system in the physiological response to transient common carotid artery occlusion and reperfusion
TLDR
The BCCAO/R stimulated early molecular changes that can be easily traced in brain tissue and plasma, and that are indicative of the tissue physiological response to the reperfusion-induced oxidative stress and inflammation, which suggest that the positive modulation of the ECS and the increase of proinflammatory substances are directly correlated events.
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References

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TLDR
It is shown that exogenously administered AEA dose-dependently reduced neuronal damage in neonatal rats injected intracerebrally with the Na+/K+-ATPase inhibitor ouabain, and the data seem to question a possible role of the endogenous cannabinoid system in establishing a brain defense system in the authors' model.
Anandamide content is increased and CB1 cannabinoid receptor blockade is protective during transient, focal cerebral ischemia
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Cannabinoid CB2 Receptor Activation Decreases Cerebral Infarction in a Mouse Focal Ischemia/Reperfusion Model
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CB2 activation is associated with a Reduction in white blood cell rolling and adhesion along cerebral vascular endothelial cells, a reduction in infarct size, and improved motor function after transient focal ischemia.
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