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.
Keywords: BDNF; Depression; Inflammation; Lipopolysaccharide; Salidroside.
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