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NLRP3 炎性小体抑制减轻糖尿病小鼠脑缺血再灌注损伤。

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

机构信息

Department of Anesthesiology, Zhujiang Hospital of Southern Medical University, Guangzhou, China.

Department of Anesthesiology, The Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong, China.

出版信息

Neural Plast. 2018 Apr 24;2018:9163521. doi: 10.1155/2018/9163521. eCollection 2018.

DOI:10.1155/2018/9163521
PMID:29853850
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5941718/
Abstract

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-1, 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.

摘要

NLRP3 炎性小体的持续激活与糖尿病和中风密切相关。然而，目前尚不清楚 NLRP3 炎性小体在糖尿病性中风中是否发挥重要作用。我们旨在研究 NLRP3 炎性小体在糖尿病脑缺血再灌注损伤小鼠中的作用及其潜在机制。通过高脂肪饮食和链脲佐菌素（STZ）诱导 2 型糖尿病小鼠模型。糖尿病小鼠在大脑中动脉闭塞（MCAO）和再灌注前 60 分钟接受 MCC950（NLRP3 的特异性分子抑制剂）或载体。MCC950 降低了脑缺血再灌注后 24 小时的神经功能缺损评分，并提高了糖尿病小鼠脑缺血再灌注损伤的 28 天存活率。此外，我们发现糖尿病脑缺血再灌注损伤小鼠核心缺血区 NLRP3、IL-1 和半胱天冬酶-1 的 mRNA 转录水平显著放大，而 MCC950 预处理明显减弱了这种现象。总之，NLRP3 炎性小体参与了糖尿病性中风的复杂疾病。NLRP3 特异性抑制剂 MCC950 改善了糖尿病脑缺血再灌注损伤小鼠的脑缺血再灌注损伤，并提高了缺血性中风恢复阶段的 28 天存活率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f36/5941718/7f48cf22771b/NP2018-9163521.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f36/5941718/80b5f41b76d0/NP2018-9163521.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f36/5941718/7f48cf22771b/NP2018-9163521.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f36/5941718/80b5f41b76d0/NP2018-9163521.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f36/5941718/b9b24515f39e/NP2018-9163521.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f36/5941718/88cfe72e9ca1/NP2018-9163521.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f36/5941718/8ac7b63b1719/NP2018-9163521.004.jpg
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