Inhibitory effect of extratable petroleum ether of Polyrhachis vicina Roger on neuroinflammatory response in depressed rats
10.16438/j.0513-4870.2017-1010
- VernacularTitle:拟黑多刺蚁石油醚部位对抑郁大鼠神经炎症反应的抑制作用
- Author:
Xin ZHANG
1
;
Qian LONG
1
;
Shi-feng CHU
2
;
Sha-sha WANG
1
;
Gui-ning WEI
3
;
Dong-mei LI
3
;
Nai-hong CHEN
1
Author Information
1. College of Chinese Materia Medica, Shanxi University of Chinese Medicine, Taiyuan 030619, China
2. Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China
3. Guangxi Institute of Chinese Medicine and Pharmaceutical Sciences, Nanning 530022, China
- Publication Type:SPECIAL REPORTS
- Keywords:
Polyrhachis vicina Roger;
depression;
cytokine;
NF-κB p65
- From:
Acta Pharmaceutica Sinica
2018;53(7):1042-1047
- CountryChina
- Language:Chinese
-
Abstract:
The main ingredient of extractable petroleum ether of Polyrhachis vicina Roger (EPPR) is octadecene unsaturated fatty acids. Mounting evidence supports that N-3 polyunsaturated fatty acids can attenuate neuroinflammation, reduce oxidative stress, then protect neurons. In order to explore the effect of EPPR on the inflammatory response of depressed rats, the model of depression was established by chronic unpredictable mild stress (CUMS). Sucrose preference test, forced swimming test were employed to investigate the anti-depressive effect of EPPR in rat. The activation of glial cells and astrocytes in the prefrontal cortex of depressed rats was observed by immunofluorescence. The levels of inflammatory factors were measured by Quantitative Real-time PCR. NF-κB was detected by immunoblotting. EPPR could significantly improve the depressive behavior of rats, decrease NF-κB translocation to the compartment of nucleus, down-regulate the pro-inflammatory cytokines IL-1β, TNF-α and indoleamine 2,3-dioxygenase (IDO) gene expression levels, inhibit the activation of microglia and astrocytes in depressed rats. These results suggest that EPPR could notably ameliorate inflammation induced by chronic stress, and the protective effect might be linked to the regulation of NF-κB p65.
