TNF-α诱导的血脑屏障的改变在急性心肌梗死后抑郁中的作用及机制探讨

Exploration on Effect and Mechanism of TNF-α Induced Alterations of the Blood-brain Barrier in Depression after Myocardial Infarction

心肌梗死后抑郁障碍的发生使人们认识到心脑在病理上存在一定联系。患有急性心肌梗死患者具有三倍的风险发展为抑郁。反之,抑郁症状可以增加心血管病的风险。这两种情况的并存与患者预后不良有密切关系。尽管导致这一交互作用的潜在机制尚不明确,但是有人认为炎性反应可能在其中发挥巨大作用。急性心肌梗死诱发的外周组织细胞因子的释放可以引发脑内皮渗漏和血脑屏障完整性的破坏,因此可以诱发神经炎性反应的发生。本文试图从心肌梗死后抑郁发生机制中揭示心脑之间的关系,并为临床心肌梗死后抑郁的治疗提供生物学依据。

The incidence of depression after myocardial infarction brings people to realize that there is a cardio-cerebral pathologi-cal connection.Patients experiencing an acute myocardial infarction （ AMI） have a three times higher chance to develop depres-sion.Vice versa,depressive symptoms increase the risk of cardiovascular incidents.The co-existence of both conditions is associated with substantially worse prognosis.Although the underlying mechanism of the interaction is largely unknown, inflammation is thought to be of pivotal importance.AMI-induced peripheral cytokines release may cause cerebral endothelial leakage and the integ-rity of the blood-brain barrier damage and hence induces a neuroinflammatory reaction.The neuroinflammation may persist even longer after the initial peripheral inflammation has been subsided.This paper attempts to reveal the relationship between the heart and brain from the mechanism of depression after myocardial infarction and provide a biological basis for the treatment of depression after myocardial infarction for clinical application.