Inhibition of NLRP3 Inflammasome Ameliorates Cerebral Ischemia-Reperfusion Injury in Diabetic Mice

Bibliographic Details
Title: Inhibition of NLRP3 Inflammasome Ameliorates Cerebral Ischemia-Reperfusion Injury in Diabetic Mice
Authors: Pu Hong, Feng-Xian Li, Ruo-Nan Gu, Ying-Ying Fang, Lu-Ying Lai, Yong-Wei Wang, Tao Tao, Shi-Yuan Xu, Zhi-Jian You, Hong-Fei Zhang
Source: Neural Plasticity, Vol 2018 (2018)
Publisher Information: Hindawi Limited, 2018.
Publication Year: 2018
Collection: LCC:Neurosciences. Biological psychiatry. Neuropsychiatry
Subject Terms: Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
More Details: Sustained activation of NLRP3 inflammasome is closely related to diabetes and stroke. However, it is unknown whether NLRP3 inflammasome plays an essential role in stroke in diabetes. We aim to investigate the effect and the potential mechanism of NLRP3 inflammasome in diabetic mice with cerebral ischemia-reperfusion injury. A type 2 diabetic mouse model was induced by a high-fat diet and streptozotocin (STZ). Diabetic mice received MCC950 (the specific molecule NLRP3 inhibitor) or vehicle 60 minutes before the middle cerebral artery occlusion (MCAO) and reperfusion. MCC950 reduced the neurological deficit score of 24 h after cerebral ischemia reperfusion and improved the 28-day survival rate of cerebral ischemia-reperfusion injury in diabetic mice. Furthermore, we found that the mRNA transcription levels of NLRP3, IL-1β, and caspase-1 in the core ischemic area were remarkably amplified in diabetic mice with cerebral ischemia-reperfusion injury, whereas this phenomenon was obviously attenuated by MCC950 pretreatment. In conclusion, the NLRP3 inflammasome was involved in the complex diseases of diabetic stroke. MCC950, the NLRP3 specific inhibitor, ameliorated diabetic mice with cerebral ischemia-reperfusion injury and improved the 28-day survival rate during the recovery stage of ischemic stroke.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2090-5904
1687-5443
Relation: https://doaj.org/toc/2090-5904; https://doaj.org/toc/1687-5443
DOI: 10.1155/2018/9163521
Access URL: https://doaj.org/article/8cea57936a7041f8851b88f9e1953d42
Accession Number: edsdoj.8cea57936a7041f8851b88f9e1953d42
Database: Directory of Open Access Journals
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More Details
ISSN:20905904
16875443
DOI:10.1155/2018/9163521
Published in:Neural Plasticity
Language:English