Macrophage-NLRP3 Inflammasome Activation Exacerbates Cardiac Dysfunction after Ischemic Stroke in a Mouse Model of Diabetes

• 作者: Feng-Xian Li Guan-Shan Wei Hong-Bin Lin Hong-Fei Zhang Pu Hong Qian-Qian Zhang Shi-Yuan Xu Wen-Bin Liang Wen-Jing Guo Ya-Qian Weng Zhi-Jian You
• 来源期刊: 神经科学通报（英文版）
• 年，卷（期）: 2020,（9）
• 所属期刊栏目: Original Articles
• 页码范围: 1035-1045
• 页数: 11页
• 语种: 英文

摘要

Ischemic stroke is one of the leading causes of death worldwide.In the post-stroke stage,cardiac dysfunction is common and is known as the brain-heart interaction.Diabetes mellitus worsens the post-stroke outcome.Stroke-induced systemic inflammation is the major causative factor for the sequential complications,but the mechanism underlying the brain-heart interaction in diabetes has not been clarified.The NLRP3 (NLR pyrin domain-containing 3) inflammasome,an important component of the inflammation after stroke,is mainly activated in M1-polarized macrophages.In this study,we found that the cardiac dysfunction induced by ischemic stroke is more severe in a mouse model of type 2 diabetes.Meanwhile,M1-polarized macrophage infiltration and NLRP3 inflammasome activation increased in the cardiac ventricle after diabetic stroke.Importantly,the NLRP3 inflammasome inhibitor CY-09 restored cardiac function,indicating that the Ml-polarized macrophage-NLRP3 inflammasome activation is a pathway underlying the brain-hert interaction after diabetic stroke.