Title:Curcumin Alleviates Cerebral Ischemia-reperfusion Injury by Inhibiting NLRP1-dependent Neuronal Pyroptosis
Volume: 18
Issue: 2
Author(s): Lifa Huang*, Xu Li, Yajun Liu, Xiaolong Liang, Hui Ye, Chao Yang, Lin Hua and Xin Zhang*
Affiliation:
- Department of Neurosurgery, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006,China
- Department of Neurosurgery, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006,China
Keywords:
Cerebral ischemia-reperfusion injury, curcumin, pyroptosis, NLRP1, blood reperfusion, brain.
Abstract:
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, However, the mechanism is not clear.
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.