Cudrania cochinchinensis attenuates amyloid β protein-mediated microglial activation and promotes glia-related clearance of amyloid β protein

Background: microglial inflammation may significantly contribute to the pathology of alzheimer's disease. to examine the potential of cudrania cochinchinensis to ameliorate amyloid β protein (aβ)-induced microglia activation,bv-2 microglial cell line,and the ramified microglia in the primary glial mixed cultured were employed. results: lipopolysaccharide (lps),interferon-γ (ifn-γ),fibrillary aβ (faβ),or oligomeric aβ (oaβ) were used to activate microglia. lps and ifn-γ,but not aβs,activated bv-2 cells to produce nitric oxide through an increase in inducible nitric oxide synthase (inos) expression without significant effects on cell viability of microglia. faβ,but not oaβ,enhanced the ifn-γ-stimulated nitric oxide production and inos expression.the ethanol/water extracts of cudrania cochinchinensis (cc-ew) and the purified isolated components (i.e. cca to ccf) effectively reduced the nitric oxide production and inos expression stimulated by ifn-γ combined with faβ. on the other hand,oaβ effectively activated the ramified microglia in mixed glial culture by observing the morphological alteration of the microglia from ramified to amoeboid. cc-ew and ccb effectively prohibit the aβ-mediated morphological change of microglia. furthermore,cc-ew and ccb effectively decreased aβ deposition and remained aβ in the conditioned medium suggesting the effect of cc-ew and ccb on promoting aβ clearance. results are expressed as mean ± s.d. and were analyzed by anova with post-hoc multiple comparisons with a bonferroni test. conclusions: the components of cudrania cochinchinensis including cc-ew and ccb are potential for novel therapeutic intervention for alzheimer's disease. © 2013 wang et al.; licensee biomed central ltd.