Berberine suppresses amyloid-beta-induced inflammatory response in microglia by inhibiting nuclear factor-kappaB and mitogen-activated protein kinase signalling pathways

Objectives The neuroinflammation induced by amyloid-beta peptide (A beta) is one of the key events in Alzheimer's disease (AD) progress in which microglia are the main cells involved. Berberine, one of the major constituents of Chinese herb Rhizoma coptidis, is known for its anti-inflammatory, anti-oxidative and anti-microbial activity. In this study, we examined the effects and possible underlying mechanisms of berberine in A beta-induced neuroinflammation using murine primary microglia cells and cultured BV2 microglia cells. Methods The effects of berberine on A beta-stimulated inflammatory factor expression and secretion were examined using RT-PCR and ELISA analysis. The signal pathways involved in berberine's effects were also investigated using Western blot and immunofluorescence analysis. Results In primary microglial and BV2 cells, berberine treatment significantly inhibited A beta-stimulated production of interleukin-6 and monocyte chemotactic protein-1. Berberine treatment down-regulated the expression of cyclo-oxygenase-2 and induced nitric oxide synthase in these cells. Moreover, berberine strongly inhibited the nuclear factor-kappaB (NF-?B) activation, presumably through blocking the phosphoinositide 3-kinase/protein kinase B and mitogen-activated protein kinase signalling pathways. Conclusions Our data indicated berberine is a potent suppressor of neuroflammation, presumably through inhibition of NF-?B activation, and suggested berberine has therapeutic potential for the treatment of neuroinflammation that is involved in neurological diseases such as AD.