Trehalose Alleviates PC12 Neuronal Death Mediated by Lipopolysaccharide-Stimulated BV-2 Cells via Inhibiting Nuclear Transcription Factor NF-κB and AP-1 Activation

• DOI: 10.1007/s12640-014-9487-7
• Publication Date: 2014-08-14T14:20:13Z
• Authors: Qing He; Ying Wang; Wei Lin; Qiong Zhang; Jue Zhao; Feng-Tao Liu; Yi-Lin Tang; Bao-guo Xiao; Jian Wang
• Keywords: Lipopolysaccharides; Neurons; 0301 basic medicine; Cell Death; NF-kappa B; Trehalose; PC12 Cells; Cell Line; Rats; Transcription Factor AP-1; Mice; 03 medical and health sciences; Neuroprotective Agents; Culture Media, Conditioned; Animals; Cytokines; Microglia

Inflammation is implicated in the pathogenesis of Parkinson's disease (PD). Trehalose is a disaccharide which exhibits a variety of effects like anti-aggregation, autophagy enhancement in PD. It has also been known to suppress inflammation in many experimental models, involving endotoxin shock, murine dry eye and subarachnoid hemorrhage. However, whether trehalose has an anti-inflammation effect on PD is largely unknown. In the present study, we found trehalose inhibited generation of interleukin-1β, interleukin-6, tumor necrosis factor-α, and nitric oxide in the conditioned medium released from lipopolysaccharide (LPS)-stimulated BV-2 cells. LPS-induced nuclear transcription factors of NF-κB and AP-1 activation were also inhibited by trehalose. Then the conditioned medium of BV-2 cells was applied to PC12 neurons. As a result, both MTT and LDH indicated that trehalose decreased PC12 neuronal death. TUNEL assay showed that trehalose suppressed apoptosis of PC12 neurons. These results implied that trehalose exerted a protective effect on PC12 neurons against the neurotoxic effect triggered by BV-2 microglial activation through inhibiting NF-κB and AP-1 activation and inflammatory mediators and cytokines production in BV-2 cells.