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Cannabidiol prevents a post-ischemic injury progressively induced by cerebral ischemia via a high-mobility group box1-inhibiting mechanism.
Delayed treatment with cannabidiol has a cerebroprotective action via a cannabinoid receptor-independent myeloperoxidase-inhibiting mechanism.
Cannabidiol prevents cerebral infarction via a serotonergic 5-hydroxytryptamine1A receptor-dependent mechanism.
Neuroprotective effect of gamma-glutamylethylamide (theanine) on cerebral infarction in mice.
Cannabidiol prevents infarction via the non-CB1 cannabinoid receptor mechanism.
Preferential involvement of Na?/Ca²? exchanger type-1 in the brain damage caused by transient focal cerebral ischemia in mice.
Repeated treatment with cannabidiol but not Delta9-tetrahydrocannabinol has a neuroprotective effect without the development of tolerance.
High-cholesterol feeding aggravates cerebral infarction via decreasing the CB1 receptor.
Involvement of GABA(A) receptors in the neuroprotective effect of theanine on focal cerebral ischemia in mice.
Delayed treatment with minocycline ameliorates neurologic impairment through activated microglia expressing a high-mobility group box1-inhibiting mechanism.
Infarction, Middle Cerebral Artery
Deficient eNOS phosphorylation is a mechanism for diabetic vascular dysfunction contributing to increased stroke size.
Effects of Postconditioning on Neurogenesis and Angiogenesis During the Recovery Phase After Focal Cerebral Ischemia.
Infarction Middle Cerebral Artery