Bee venom ameliorates lipopolysaccharide-induced memory loss by preventing NF-kappaB pathway
Journal of Neuroinflammation 2015, 12:124
Accumulation of beta-amyloid and neuroinflammation trigger Alzheimer's disease. We previously found that lipopolysaccharide (LPS) caused neuroinflammation with concomitant accumulation of beta-amyloid peptides leading to memory loss.
A variety of anti-inflammatory compounds inhibiting nuclear factor kappaB (NF-ÎºB) activation have showed efficacy to hinder neuroinflammation and amyloidogenesis. We also found that bee venom (BV) inhibits NF-ÎºB.
Methods: A mouse model of LPS-induced memory loss used administration of BV (0.8 and 1.6 Î¼g/kg/day, i.p.) to ICR mice for 7 days before injection of LPS (2.5 mg/kg/day, i.p.).
Memory loss was assessed using a Morris water maze test and passive avoidance test. For in vitro study, we treated BV (0.5, 1, and 2 Î¼g/mL) to astrocytes and microglial BV-2 cells with LPS (1 Î¼g/mL).
Results: We found that BV inhibited LPS-induced memory loss determined by behavioral tests as well as cell death.
BV also inhibited LPS-induced increases in the level of beta-amyloid (AÎ²), Î²-and Î³-secretases activities, NF-ÎºB and its DNA-binding activity and expression of APP, and BACE1 and neuroinflammation proteins (COX-2, iNOS, GFAP and IBA-1) in the brain and cultured cells. In addition, pull-down assay and molecular modeling showed that BV binds to NF-ÎºB.
Conclusions: BV attenuates LPS-induced amyloidogenesis, neuroinflammation, and therefore memory loss via inhibiting NF-ÎºB signaling pathway.
Thus, BV could be useful for treatment of Alzheimer's disease.