原肌球蛋白受体激酶B
内科学
内分泌学
萧条(经济学)
脑源性神经营养因子
神经营养因子
慢性应激
认知障碍
医学
认知
神经科学
心理学
受体
宏观经济学
经济
作者
Shang-Zhi Liu,Jie Yang,Linlin Chen,Ping Wang,Li Lin
标识
DOI:10.1016/j.ejphar.2022.175385
摘要
Depression is a common disorder with a complex pathogenesis. Tanshinone IIA (TAN IIA) is a botanical agent with neuroprotective and antidepressant properties.To examine the effects of TAN IIA on chronic unpredictable mild stress (CUMS)-induced depression-like behavior and cognitive impairment in rats.Rats were exposed to CUMS for 4 weeks, followed by the oral administration of TAN IIA, Deanxit (DEAN), or normal saline for an additional 4 weeks. The control rats were fed with regular chow and administered with normal saline for 4 weeks. Behavioral tests were performed to assess the effects of TAN IIA on depression-like behavior and cognitive impairment in rats with CUMS. The morphology of dendrites was analyzed by Golgi staining. Immunofluorescence staining was performed to determine protein localization.TAN IIA treatment ameliorated CUMS-induced depression-like behavior and cognitive impairment in rats. TAN IIA treatment also reversed the effects of CUMS on dendritic complexity and the levels of gamma-aminobutyric acid (GABA) in the hippocampus and prefrontal cortex. Rats with CUMS showed decreased levels of brain-derived neurotrophic factor (BDNF) and phosphorylated tropomyosin receptor kinase B (TrkB), upregulated expression of GABA transporter 1 (GAT1), and reduced expression of synaptic proteins in the hippocampus, while TAN IIA treatment significantly diminished the effects of CUMS exposure. In addition, GAT1 was colocalized with N-methyl-D-aspartate receptor 2B.TAN IIA ameliorates CUMS-induced depression-like behavior and cognitive impairment in rats by regulating the BDNF/TrkB/GAT1 signaling pathway, suggesting that TAN IIA may be a candidate drug for the treatment of depression.
科研通智能强力驱动
Strongly Powered by AbleSci AI