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Alternative TitleInflammatory mechanism on pathogenic fire derived from stagnation of liver-qi in anxiety rats
赵振武1; 郭蓉娟2; 顾丽佳3; 史华伟4; 邓潇斐3; 郭晓2; 袁清洁5; 郭建友3
First Author赵振武
Contribution Rank3

目的:从炎症反应相关信号探讨焦虑症肝郁化火的形成机制。方法:采用单笼饲养和不确定性空瓶饮水应激建立肝郁化火焦虑模型。Wistar大鼠随机分成空白对照组、模型组,在应激第7天和14天用高架十字迷宫试验、旷场实验及明暗箱实验行为学评价,ELISA法测定外周血清和杏仁核中炎症因子IL-1β、IL-6、TNF-α、IL-10含量及mRNA表达水平。结果:模型组肝郁化火时(应激第14天)血清和杏仁核IL-1β、IL-6、TNF-α含量均显著增加(P<0.01),IL-10含量显著减少(P<0.01),杏仁核上述炎症因子mRNA与之类似,而肝气郁结时(应激第7天)仅有血清IL-1β、TNF-α含量及杏仁核IL-1β、IL-6 mRNA增加(P<0.05)。结论:在肝郁化火时,杏仁核及外周血炎症反应相关信号呈活化状态,促炎反应增加和抗炎反应减弱,免疫失衡,焦虑症肝郁化火实质是炎症。

Other Abstract

To explore the formation mechanism of pathogenic fire derived from stagnation of liverqi (PFSL) in anxiety disorder through the inflammation related signal. Methods: Single cage rearing and stress of uncertain bottle of drinking water was used to prepare anxiety disorder rat model due to PFSL. Wistar rats were randomly divided into control group and model group. Elevated plus maze test, open field test and light/dark box test was used to assess anxiety behavior at seventh day and fourteenth day. Levels of inflammatory factors (IL-1β, IL-6, TNF-α, IL-10) and mRNA expression in peripheral blood and amygdala were detected by the ELISA method. Results: The levels of IL-1β, IL-6 and TNF-α in the serum and amygdala of model rats at the PFSL on the 14th day increased significantly (P<0.01) and the level of IL-10 decreased significantly observably (P<0.01). The mRNA expression level of these inflammatory factors in the amygdala was similar to the former. However, on the seventh day the levels of IL-1β and TNF-α in the serum and IL-1β and IL-6 in the amygdala at stagnation of liver qi increased merely (P<0.05). Conclusion: During anxiety disorder due to PFSL, the inflammatory response signals both in amygdala and serum of model rats deviated from normal range, which indicates that the inflammatory response at these sites is activated and inflammatory factors are involved in the process of injury and the neuroendocrine immunity network regulation. Proinflammatory response increases and anti-inflammatory response decreases. The essence of anxiety disorder with PFSL is inflammation.

Keyword肝郁化火 焦虑症 血清 杏仁核 炎症因子
Source Publication中华中医药杂志
Indexed ByCSCD
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Document Type期刊论文
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GB/T 7714
赵振武,郭蓉娟,顾丽佳,等. 焦虑症肝郁化火的动物实验炎症机制研究[J]. 中华中医药杂志,2020,35(4):2010-2013.
APA 赵振武.,郭蓉娟.,顾丽佳.,史华伟.,邓潇斐.,...&郭建友.(2020).焦虑症肝郁化火的动物实验炎症机制研究.中华中医药杂志,35(4),2010-2013.
MLA 赵振武,et al."焦虑症肝郁化火的动物实验炎症机制研究".中华中医药杂志 35.4(2020):2010-2013.
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