临床现象发现社会支持的缺乏可明显增加抑郁症发生风险，影响抑郁症转归。而社会支持可缓冲应激对情绪、认知及生理功能的损害，改善抑郁情绪，但目前其机制尚不明了且缺乏相应成熟的社会支持动物模型。最新研究提示中枢神经系统NLRP3炎症小体、IL-18、NF-κB炎症因子可能与抑郁症发生及转归有关，我们前期研究发现CRMP2介导神经可塑性参与抑郁的发生，但社会支持模型中神经炎症及神经可塑性机制尚不明确。本项目拟建立社会支持动物模型，探讨社会支持对抑郁个体行为的影响，研究神经炎症及神经可塑性病理生理变化；进一步沉默或激活IL-18炎症通路，检测此炎症通路改变对社会支持效应的影响及神经可塑性的改变；并从细胞学进行验证。由此，从NLRP3炎症小体/IL-18/NF-κB炎症通路介导的神经炎症与CRMP2介导的神经可塑性角度，探索抑郁症及社会支持的病理生理机制，为抑郁症防治提供新策略及新靶点。

Clinical phenomena revealed that the lack of social support can significantly increase the risk of depression, affecting the outcome of depression. However, social support can significantly buffer the damage of emotional, cognitive and physiological functions，improve the depression, and promote stress resistance,but the mechanism is still unclear.And now, there is no corresponding mature social support animal model. The latest research suggest that nervous system NLRP3 inflammasome, IL-18 and NF-κB inflammatory factors may be related to the occurrence and prognosis of depression. Our previous researches show that CRMP2-mediated neuroplasticity are involved in the occurrence of depression, but the mechanism of neuroinflammation and neuroplasticity in the social support model is not clear. The aim of this research is to establish an animal model of social support to explore the impact of social support on the behavior of depressed individuals，to study the pathophysiological changes of neuroinflammation and neuroplasticity. Furthermore, by silencing or activating the IL-18 pathway, we may discuss how the change in IL-18 pathway effect social support and CRMP2-mediated neuroplasticity. Therefore, from the perspective of NLMP3 inflammasome / IL-18 / NF-κB inflammatory pathway-mediated neuroinflammation and CRMP2-mediated neuroplasticity, we hope to open a new angle to explore the pathophysiological mechanisms of depression and social support. Our research may provide helpful exploration for the prevention and treatment of depression.