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Background and PurposeCurcumin, a natural antioxidant isolated from Curcuma longa, has been reported to exert neuroprotective effect in animal models of ischemic stroke. However, the underlying mechanism is still not fully understood. The purpose of this study was to investigate the effect of curcumin treatment on neuronal apoptosis in the periinfarct cortex after cerebral ischemia/reperfusion (I/R) injury and in mouse N2a cells after oxygen‐glucose deprivation/reoxygenation (OGD/R) injury and its underlying mechanism.MethodsThe cerebral I/R injury was established by 1‐hr middle cerebral artery occlusion (MCAO) and reperfusion in mice. Infarct volume was determined by TTC staining, and neurological score was evaluated by mNSS. Cell morphology in the ischemic boundary zone were detected by HE staining. The number and apoptotic rate of neurons in ischemic boundary zone were assayed by immunohistochemistry and TUNEL, respectively. Mouse neuroblastoma N2a cells were subjected to OGD/R. Cell viability was assessed with CCK‐8. The mitochondrial membrane potential was measured using JC‐1 staining. The expression of Bax, Bcl‐2, and caspase‐3 was detected using Western blotting. Besides, cellular distribution of Bax was determined by immunofluorescence assays.ResultsCurcumin treatment reduced infarct volume, improved neurological function, alleviated the morphological damage of neurons, and increased neuronal survival rate after I/R injury in vivo. Moreover, curcumin treatment improved cell viability, reduced cell apoptosis, increased Bcl‐2 protein levels while decreased Bax and caspase‐3 expressions in mouse N2a cells after OGD/R injury. Besides, curcumin treatment inhibited Bax activation and maintained mitochondrial membrane integrity.ConclusionCurcumin promotes neuron survival in vivo and in vitro to exert neuroprotective effects against ischemia injury. Moreover, our results for the first time demonstrated curcumin inhibited ischemia‐induced mitochondrial apoptosis via restricting Bax activation, which may be one of the possible mechanisms underlying the neuroprotective effects of curcumin.

Background and PurposeSubarachnoid hemorrhage (SAH)‐induced cerebral vasospasm and early brain injury is a fatal clinical syndrome. Cerebral vasospasm and early brain injury are associated with inflammatory response and oxidative stress. Whether curcumin, which plays important roles to regulate inflammatory cytokines and inhibit oxidative stress, inhibits SAH‐induced inflammation and oxidative stress are largely unknown.MethodsAdult male rats underwent autologous blood injection into prechiasmatic cistern to induce SAH. Curcumin (150 mg/kg) was administered at 0.5, 24 and 48 hr post‐SAH. Mortality calculation and neurological outcomes as well as morphological vasospasm of anterior cerebral artery were studied. Superoxide dismutase, lipid peroxidation, and inflammatory cytokines (MCP‐1 and TNF‐α) expression in prefrontal region were quantified. Furthermore, p65 and phosphor‐p65 were quantitatively analyzed.ResultsCurcumin remarkedly reduced mortality and ameliorated neurological deficits after SAH induction (p < .05); morphological results showed that cerebral vasospasm in curcumin‐treated group was mitigated (p < .05). SAH‐induced MCP‐1 and TNF‐α overexpression were inhibited in curcumin‐treated group (p < .05). Importantly, phosphor‐p65 was significantly inhibited after curcumin treatment (p < .05).ConclusionsCurcumin can inhibit SAH‐induced inflammatory response via restricting NF‐κB activation to alleviate cerebral vasospasm and early brain injury.