![conference banner](/images/conference-banner.jpeg)
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.
Keywords: Cerebral ischemia-reperfusion injury, curcumin, pyroptosis, NLRP1, blood reperfusion, brain.
[http://dx.doi.org/10.1177/1971400917690166] [PMID: 28424015]
[http://dx.doi.org/10.1186/s13063-017-1874-y] [PMID: 28399935]
[http://dx.doi.org/10.1111/j.1365-2362.2011.02546.x] [PMID: 21623777]
[http://dx.doi.org/10.1189/jlb.1109766] [PMID: 20130219]
[http://dx.doi.org/10.1007/s002210050424] [PMID: 9655236]
[http://dx.doi.org/10.1016/j.jep.2014.03.057] [PMID: 24690773]
[http://dx.doi.org/10.1007/978-981-13-1426-1_25] [PMID: 30259377]
[http://dx.doi.org/10.1182/blood-2012-06-440057] [PMID: 22936662]
[http://dx.doi.org/10.1016/j.brainres.2010.01.079] [PMID: 20138164]
[http://dx.doi.org/10.1007/s12035-017-0467-9] [PMID: 28255908]
[http://dx.doi.org/10.1038/nature11729] [PMID: 23254930]
[http://dx.doi.org/10.1111/bpa.12467] [PMID: 27880990]
[http://dx.doi.org/10.1007/s00281-007-0078-z] [PMID: 17690885]
[http://dx.doi.org/10.1016/j.cell.2010.01.040] [PMID: 20303873]
[http://dx.doi.org/10.1038/nri2690] [PMID: 20098460]
[http://dx.doi.org/10.1073/pnas.0913087107] [PMID: 20133635]
[http://dx.doi.org/10.1073/pnas.0707370105] [PMID: 18337499]
[http://dx.doi.org/10.1038/ng1724] [PMID: 16429160]
[http://dx.doi.org/10.1038/nature18590] [PMID: 27281216]
[http://dx.doi.org/10.15252/embj.201694696] [PMID: 27418190]
[http://dx.doi.org/10.1369/jhc.6A7101.2006] [PMID: 17164409]
[http://dx.doi.org/10.1038/cddis.2013.326] [PMID: 24008734]
[http://dx.doi.org/10.1007/s12035-013-8551-2] [PMID: 24014157]
[http://dx.doi.org/10.1016/j.bbi.2015.06.016] [PMID: 26162710]
[http://dx.doi.org/10.3892/mmr.2015.3322] [PMID: 25673156]
[http://dx.doi.org/10.1007/s13105-016-0515-3] [PMID: 27534650]
[http://dx.doi.org/10.2147/DDDT.S194182] [PMID: 31040648]
[http://dx.doi.org/10.1002/brb3.921] [PMID: 29484272]
[http://dx.doi.org/10.1159/000489241] [PMID: 29694958]
[http://dx.doi.org/10.3390/foods6100092] [PMID: 29065496]
[http://dx.doi.org/10.1016/j.neuroscience.2016.07.012] [PMID: 27423629]
[http://dx.doi.org/10.3390/nu9060578] [PMID: 28587282]
[http://dx.doi.org/10.4049/jimmunol.1701495] [PMID: 29549176]
[http://dx.doi.org/10.4049/jimmunol.1201065] [PMID: 22753929]
[http://dx.doi.org/10.1186/s12974-014-0233-0] [PMID: 25626361]
[http://dx.doi.org/10.1016/j.lfs.2019.116599] [PMID: 31247210]
![Wayfinder Image](/images/wayfinder.jpg)