ABSTRACT
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.
ABSTRACT
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.
ABSTRACT
Objective To explore the relationship of vascular endothelial growth factor(VEGF),IFN-? and IL-4 and effect of Bude-sonide on their in asthmatic rats.Methods Thirty-six male SD rats were randomly divided into 3 groups:asthma group,Budesonide-treatment group and control group.On the first day of the experiment and the 8th day,the rat models of the asthma group and Budesonid treatment group were allergized by the OVA/Al(OH)3 through intraperitoneal injection,respectively.And starting from the 15th day,they were challenged by the OVA through atomization for 2 weeks.Control group was allergized and challenged by NS atomization.Budesonid treatment group was interfered in Budesonide inhalation before suscitation in 0.5 h.After 12 h the same inhal done was again in Budesonide group.Twenty-four hours after the last challenge,the rats in 3 groups were sacrificed,and blood and bronchoalveolar lavage fluid(BALF) were collected.The concentrations of IL-4,IFN-? and VEGF in serum and BALF were measured by enzyme-linked immunosorbent assay.Results The concentrations of IL-4 in serum and BALF in asthma group and Budesonide treatment group were significantly increased than those in control group(P