title: Berberine suppresses amyloid-beta-induced inflammatory response in microglia by inhibiting nuclear factor-kappaB and mitogen-activated protein kinase signalling pathways.
abstract: OBJECTIVE
  The neuroinflammation induced by amyloid-beta peptide (Aβ) 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 Aβ-induced neuroinflammation using murine primary microglia cells and cultured BV2 microglia cells.
  
  
  METHODS
  The effects of berberine on Aβ-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 Aβ-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-κB) 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-κB activation, and suggested berberine has therapeutic potential for the treatment of neuroinflammation that is involved in neurological diseases such as AD.
authors.affiliation: Institute of Medical Genetics and Key Laboratory for Experimental Teratology of the Ministry of Education, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China.
authors.forename: Liyun
authors.initials: L
authors.lastname: Jia
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Zhen
authors.initials: Z
authors.lastname: Song
authors.forename: Xiaohua
authors.initials: X
authors.lastname: Pan
authors.forename: Liang
authors.initials: L
authors.lastname: Chen
authors.forename: Xing
authors.initials: X
authors.lastname: Cui
authors.forename: Molin
authors.initials: M
authors.lastname: Wang
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001599:Berberine / Q000494:pharmacology*; D015153:Blotting, Western; D002478:Cells, Cultured; D004797:Enzyme-Linked Immunosorbent Assay; D007249:Inflammation / Q000188:drug therapy / Q000473:pathology; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D051379:Mice; D017628:Microglia / Q000187:drug effects* / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D016229:Amyloid beta-Peptides; D016328:NF-kappa B; D001599:Berberine