Abstract
BackgroundMicroglial 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.ResultsLipopolysaccharide (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.ConclusionsThe components of Cudrania cochinchinensis including CC-EW and CCB are potential for novel therapeutic intervention for Alzheimer’s disease.
Highlights
Microglial inflammation may significantly contribute to the pathology of Alzheimer’s disease
The nitric oxide production induced by LPS, IFN-γ, and IFN-γ combined with fibrillary Aβ (fAβ) in BV-2 cells culture To determine the inflammatory potential of BV-2 cells, nitric oxide production was assayed after BV-2 cells were activated by different stimuli
The results show that IFN-γ combined with fAβ induced a significantly higher amount of inducible nitric oxide synthase (iNOS) expression than that induced by IFN-γ alone
Summary
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. The brain-resident macrophages, exhibits several morphological features that distinguish them from peripheral macrophages. These include ramified branches in the steady-state phenotype and the amoeboid morphology of renewed and activated phenotypes [3,4]. The property of the activated amoeboid microglia is similar to macrophages. The primary determinants of ramified phenotype and amoeboid phenotype of microglia under pathological conditions in the CNS are less well defined and may be different from those of macrophages in the peripheral tissues
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