Background:
Cerebral ischemia-reperfusion injury is caused by a blood reperfusion injury in the ischemic brain and usually occurs in the treatment stage of ischemic disease, which can aggravate brain tissue injury.
Objective:
Curcumin was reported to exert a good therapeutic effect on neural cells against ischemia-reperfusion injury, while the mechanism was unclear.
Methods:
In this study, oxygen glucose deprivation (OGD) model of fetal rat cerebral cortical neurons and the middle cerebral artery occlusion (MCAO) model of rats were employed to mimic cerebral ischemia-reperfusion injury in vitro and in vivo，respectively.
Results:
We confirmed that curcumin has a promotive effect on neuronal proliferation and an inhibitory effect on neuronal pyroptosis. Furthermore, we found that curcumin could improve cerebral infarction. The results of western blotting showed that curcumin down-regulated the expression of nucleotide-binding oligomerization domain-containing protein-, leucine-rich repeats-, and pyrin domain-containing protein 1 (NLRP1), cysteinyl aspartate-specific protease 1 (caspase-1), gasdermin D (GSDMD), IL-1β, IL-6, TNF-α, and iNOS proteins in OGD and MCAO models. NLRP1-dependent neuronal pyroptosis played an important role in cerebral ischemia-reperfusion injury.
Conclusion:
Curcumin could effectively inhibit NLRP1-dependent neuronal pyroptosis by suppressing the p38 MAPK pathway and therefore exerted neuroprotective effects against cerebral ischemia-reperfusion injury.
MAPK pathway mediates the anti‑oxidative effect of chicoric acid against cerebral ischemia‑reperfusion injury in�vivo
