Salidroside attenuates lipopolysaccharide (LPS) induced serum cytokines and depressive-like behavior in mice. (8th October 2015)

• Record Type: Journal Article
• Authors: Zhu, Lingpeng; Wei, Tingting; Gao, Jing; Chang, Xiayun; He, He; Miao, Mingxing; Yan, Tianhua
• Is Part Of: Neuroscience letters. Volume 606(2015)
• Page Start: 1
• Page End: 6
• Publication Date: 2015-10-08
• Subjects: Salidroside -- Lipopolysaccharide -- Depression -- Inflammation -- BDNF; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2015.08.025
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Salidroside increased BDNF. Salidroside decreased inflammation. Salidroside decreased depressive-like behavior. Abstract: The aim of the study was to investigate the effects and possible underlying mechanism of salidroside (Sal) on lipopolysaccharide (LPS)-induced depression-like behavior in mice. Sal (12 mg/kg and 24 mg/kg) and fluoxetine (20 mg/kg) were administered intragastrically once daily for 5 days. At the 5th day, LPS (0.5 mg/kg) was injected intraperitoneally 30 min after drug administration. Levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-α in serum were measured by ELISA. Levels of neurotransmitters like norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in the prefrontal cortex were detected by HPLC-MS. Further, brain-derived neurotrophic factor (BDNF), tropomyosin-related kinase B (TrkB) and Nuclear factor-κB (NF-κB) in hippocampal was determined by western blot analysis. Our data showed that pretreatment with Sal dramatically attenuated LPS-induced inflammatory response, decrease of NE and 5-HT levels in the prefrontal cortex. In addition, Sal increased expression levels of BNDF and TrkB. These results suggested that Sal may play a neuroprotective role through the BDNF/TrkB signaling pathway.