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 M1-polarized macrophage–NLRP3 inflammasome activation is a pathway underlying the brain–heart interaction after diabetic stroke.

中文翻译：

---

巨噬细胞-NLRP3 炎症小体激活在糖尿病小鼠模型中加剧缺血性中风后的心脏功能障碍。

缺血性中风是全球死亡的主要原因之一。在中风后阶段，心脏功能障碍很常见，被称为脑-心相互作用。糖尿病会恶化中风后的结果。中风引起的全身炎症是继发性并发症的主要致病因素，但尚未阐明糖尿病脑-心相互作用的潜在机制。NLRP3（含有NLR pyrin结构域的3）炎症小体是中风后炎症的重要组成部分，主要在M1极化的巨噬细胞中被激活。在本研究中，我们发现缺血性卒中诱发的心功能障碍在 2 型糖尿病小鼠模型中更为严重。同时，糖尿病卒中后心室中 M1 极化的巨噬细胞浸润和 NLRP3 炎性体激活增加。重要的，