Xiao Yao San Improves Depressive-Like Behavior in Rats through Modulation of β-Arrestin 2-Mediated Pathways in Hippocampus. (7th July 2014)

• Record Type: Journal Article
• Authors: Zhu, Xiaoxia; Xia, Oudong; Han, Weili; Shao, Meng; Jing, Linlin; Fan, Qin; Liu, Yuanliang; Diao, Jianxin; Lv, Zhiping; Sun, Xuegang
• Other Names: Tsim Karl Wah-Keung Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2014(2014)
• Publication Date: 2014-07-07
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2014/902516
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : Xiao Yao San (XYS) is a classical Chinese medicine formula that has been widely used to treat mood disorders for hundreds of years. To confirm the effect of XYS and better understand its underlying mechanism, high-performance liquid chromatography-mass spectrometry analysis-based quality control of XYS extracts and proteomics-based identification of differential proteins in the hippocampus were adopted in social isolation and chronic unpredictable mild stress- (CUMS-) treated rats. The depressive-like behavior of rats induced by CUMS resembled the manifestation of human depression. The upregulated corticosterone (CORT) and urocortin 2 (UCN2) levels demonstrated the existence of hypothalamic-pituitary-adrenal (HPA) axis hyperactivity. XYS was effective in ameliorating the depressive-like behavior and downregulating UCN2 and CORT. XYS decreased the expression of serine/threonine-protein phosphatase 2A subunit B and increased the expression of β -arrestin 2. The expressions of brain-derived neurotrophic factor (BDNF), tyrosine receptor kinase B (TrkB), and mammalian target of rapamycin (mTOR) were also elevated by XYS. In conclusion, XYS improves social isolation and CUMS-induced depressive-like behavior and ameliorates HPA hyperactivation through the downregulation of corticotrophin releasing hormone (CRH) receptor 2. The upregulation of BDNF/TrkB and the phosphorylation of mTOR require β -arrestin 2 as a scaffold to regulate stress signaling.