目标2
炎症
内科学
促炎细胞因子
细胞生物学
化学
上睑下垂
半胱氨酸蛋白酶1
内分泌学
先天免疫系统
作者
Elísabet Alcocer-Gómez,Cristina Ulecia-Morón,Fabiola Marín-Aguilar,Tatyana Rybkina,Nieves Casas-Barquero,Jesús Ruiz-Cabello,Bernhard Ryffel,Lionel Apetoh,François Ghiringhelli,Pedro Bullón,José Antonio Sánchez-Alcázar,Angel M. Carrión,Mario D. Cordero
标识
DOI:10.1007/s12035-015-9408-7
摘要
Depression is a major public health concern in modern society, yet little is known about the molecular link between this condition and neuroinflammation. The inflammasome complex was recently shown to be implicated in depression. The present study shows the implication of NLRP3 inflammasome in animal model of stress-induced depression. Accordingly, we show here that in the absence of a NLRP3 inflammasome, prolonged stress does not provoke depressive behaviors or microglial activation in mice or dampen hippocampal neurogenesis. Indeed, NLRP3 deletion or inhibition of microglial activation impairs the stress-induced alterations associated with depression. According to these findings in animal model, the inflammasome could be a target for new therapeutic interventions to prevent depression in patients.
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