
@article{ref1,
title="Depression-like behaviors and heme oxygenase-1 are regulated by Lycopene in lipopolysaccharide-induced neuroinflammation",
journal="Journal of neuroimmunology",
year="2016",
author="Zhang, Fang and Fu, Yanyan and Zhou, Xiaoyan and Pan, Wei and Shi, Yue and Wang, Mei and Zhang, Xunbao and Qi, Dashi and Li, Lei and Ma, Kai and Tang, Renxian and Zheng, Kuiyang and Song, Yuanjian",
volume="298",
number="",
pages="1-8",
abstract="Previous studies have demonstrated that lycopene possesses anti-inflammatory properties in the central nervous system. However, the potential role and the molecular mechanisms of lycopene in lipopolysaccharide (LPS)-challenge inflammation and depression-like behaviors has not been clearly investigated. The present study aimed to assess the effects and the potential mechanisms of lycopene on LPS-induced depression-like behaviors. Lycopene was orally administered (60mg/kg) every day for seven days followed by intraperitoneal LPS injection (1mg/kg). The Forced swim test and tail suspension test were used to detect changes in the depression-like behaviors. ELISA was used to measure the expression of interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) in the plasma. Immunoblotting was performed to measure the expression of interleukin-1β (IL-1β) and heme oxygenase-1 (HO-1) in the hippocampus. The results showed that pretreatment with lycopene could ameliorate depression-like behaviors. Moreover, lycopene relieved neuronal cell injury in hippocampal CA1 regions. Furthermore, lycopene decreased LPS-induced expression of IL-1β and HO-1 in the hippocampus together with decreasing level of IL-6 and TNF-α in the plasma. Taken together, these results suggest that lycopene can attenuate LPS-induced inflammation and depression-like behaviors, which may be involved in regulating HO-1 in the hippocampus.<br><br>Copyright © 2016 Elsevier B.V. All rights reserved.<p /> <p>Language: en</p>",
language="en",
issn="0165-5728",
doi="10.1016/j.jneuroim.2016.06.001",
url="http://dx.doi.org/10.1016/j.jneuroim.2016.06.001"
}