β2肾上腺素能信号通路调节卒中后炎症的可能分子机制  

Possible molecular mechanism of β2 adrenergic signaling pathway in regulation of inflammation after stroke

作　　者：邢方岚 闫福岭[1] 王欢[1] 邓齐文[1] 

机构地区：[1]东南大学附属中大医院神经内科,南京210009

出　　处：《国际脑血管病杂志》2016年第3期268-271,共4页International Journal of Cerebrovascular Diseases

摘　　要：感染是卒中的常见并发症之一，可严重影响患者预后。卒中后感染与机体免疫系统功能失衡密切相关，而交感神经过度激活是卒中后发生免疫抑制的重要因素。交感神经主要通过免疫细胞表面的β2肾上腺素能受体对其进行调节。有证据表明，在某些情况下β2肾上腺素能受体介导的免疫功能增强而非抑制，但其具体分子机制尚不清楚。文章对β2肾上腺素能信号通路调节卒中后炎症的分子机制进行了综述。Infection is one of the common complications of stroke. It can seriously affect the prognosis of patients. Poststroke infection is closely associated with immune system imbalance, while the excessive activation of sympathetic nerve is an important factor of the occurrence of immunosuppression after stroke. The sympathetic nerve regulates immune cels primarily via β2 adrenergic receptors on the surface of the immune cels. There is evidence to show that β2 adrenergic receptor mediated immune function enhances rather than inhibits under certain conditions, but its specific molecular mechanism is unclear. This article reviews the molecular mechanisms of β2 adrenergic signaling pathway in regulation of inflammation after stroke.

关 键 词：卒中 细菌感染 炎症 免疫抑制 受体 肾上腺素能 β2 信号转导 Receptors Adrenergic β-2 

分 类 号：R743.3[医药卫生—神经病学与精神病学]