Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

• Published in: Experimental and therapeutic medicine Vol. 15; no. 2; pp. 1574 - 1579
• Main Authors: Gao, Haiyan, Zhu, Xianghua, Xi, Yang, Li, Qun, Shen, Zhenzhong, Yang, Yongjie
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.02.2018; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Analysis; Atractylodes; Care and treatment; Complications and side effects; Cytokines; Depression (Mood disorder); Health aspects; Interleukins; Laboratory animals; Mental depression; Neurotransmitters; Prevention; Proteins; Public health; Rodents; Studies; Sucrose; United States > US; China; nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 inflammasome; depression; inflammation; atractylenolide I; interleukin-1β
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2017.5517

Atractylenolide I (AT-I), a major component of the rhizoma of Koidz., exerts a wide range of activities. The purpose of the present study was to investigate the anti-depressant-like effect of AT-I in a mouse model of chronic unpredictable mild stress (CUMS), and to explore the possible molecular mechanism involved. It was revealed that AT-I significantly ameliorated CUMS-induced depressive-like behaviors, as evidenced by increased sucrose preference as well as shortened immobility time in the forced swimming and the tail suspension test. In addition, AT-I reduced CUMS-induced decreases in the concentrations of serotonin and norepinephrine in the hippocampus. Furthermore, AT-I inhibited the activation of the nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome as well as the concentration of the pro-inflammatory cytokine interleukin (IL)-1β in the hippocampi of mice subjected to CUMS. In conclusion, the results of the present study suggested that AT-I exerts anti-depressant-like effects in a CUMS-induced model of depression in mice, the molecular mechanism of which is associated with the inhibition of NLRP3 inflammasome activation to decrease IL-1β production.