文献类型：期刊文献

英文题名：Minocycline ameliorates depressive behaviors and neuro-immune dysfunction induced by chronic unpredictable mild stress in the rat

作者：Zhang, Cai[1,2];Zhang, Yong-Ping[1,2];Li, Yu-Yu[1,2];Liu, Bai-Ping[1,2];Wang, Hao-Yin[1,2];Li, Kang-Wei[1,2];Zhao, Shannon[3];Song, Cai[1,2]

机构：[1]Guangdong Ocean Univ, Coll Food Sci & Technol, Res Inst Marine Drug & Nutr, Zhanjiang, Peoples R China;[2]Guangdong Ocean Univ, Shenzhen Inst, Marine Med Dev Ctr, Shenzhen, Guangdong, Peoples R China;[3]Univ Southern Calif, Amer Studies & Ethn, Los Angeles, CA 90089 USA

年份：2019

卷号：356

起止页码：348

外文期刊名：BEHAVIOURAL BRAIN RESEARCH

收录：SSCI(收录号：WOS:000449894800039)、SCI-EXPANDED(收录号：WOS:000449894800039)、、Scopus(收录号：2-s2.0-85053483796)、WOS

基金：This work was supported by grants to Cai Song from National Natural Science Foundation of China (No. 81471223 and No. 81171118), Project of Enhancing School with Innovation of Guangdong Ocean University (GDOU2013050110) and Guangdong Provincial Science and Technology Planning Project of Guangdong Province, China (2016A020215153 and 2016B020235001).

语种：英文

外文关键词：Chronic unpredictable mild stress; Microglial M1; Behavior; Cytokines; Neurotrophins; Minocycline

外文摘要：Activated microglia-induced neuroinflammation can stimulate the hypothalamic-pituitary-adrenal (HPA) axis to release glucocorticoids and suppress astrocyte functions, such as reducing neurotrophin production, which occur in depression. However, the balance between M1 (pro-inflammation) and M2 (anti-inflammation) microglial phenotypes and the interaction between these two glial cells are unclear in the depression. Hence, the chronic unpredictable mild stress (CUMS)-induced depression model was chosen to study depression- and anxiety-like behaviors, the concentration of corticosterone and relevant hippocampal cytokines, mRNA and protein expressions of microglial and astrocyte markers. To demonstrate the role of Ml phenotype activation in depression, the effect of microglial inhibitor minocycline on these aspects was also evaluated. Six weeks after CUMS exposure, behaviors were tested. Compared to the control group, CUMS increased serum corticosterone concentration and depression-like behaviors, like anhedonia, helplessness and anxiety. Moreover, CUMS increased microglia Ml marker CD11b expression and tumor necrosis factor (TNF)-alpha, interferon (INF)-gamma, interleukin (IL)1 beta and IL-17 concentrations, but decreased the concentration of M2 cytokines, IL-4, IL-10 and IL-13. Meanwhile, CUMS inhibited the expressions of astrocyte marker glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF) and TrKB. Minocycline (40 mg/kg, 45 days) treatment significantly attenuated CUMSinduced behavioral abnormalities, which were associated with the suppressed Ml response, restored GFAP, BDNF and its receptor expression. In conclusion, CUMS-induced depression- and anxiety-like behavior may result from an imbalance between M1 and M2 and suppressed astrocyte function. Minocycline treatment reversed M1 response, which was associated with behavioral normalization.