- 作者: Chung-Jen Wang, Chien-Chih Chen, Huey-Jen Tsay, Feng-Yi Chiang, Mine-Fong Wu and Young-Ji Shiao
- 作者服務機構: Division of Geriatrics, Cheng Hsin General Hospital, Taipei, Taiwan, R.O.C
- 中文摘要: --
- 英文摘要:
Background: Microglial inflammation may significantly contribute to the pathology of Alzheimer's disease. To examine the potential of Cudrania cochinchinensis to ameliorate amyloid beta protein (Abeta)-induced microglia activation, BV-2 microglial cell line, and the ramified microglia in the primary glial mixed cultured were employed.
Methods: Lipopolysaccharide (LPS), Interferon-gamma (IFN-gamma), fibrillary Abeta (fAbeta), or oligomeric Abeta (oAbeta) were used to activate microglia. LPS and IFN-gamma, but not Abetas, 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. fAbeta, but not oAbeta, enhanced the IFN-gamma-stimulated nitric oxide production and iNOS expression.
Results: 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-gamma combined with fAbeta. On the other hand, oAbeta 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 Abeta-mediated morphological change of microglia. Furthermore, CC-EW and CCB effectively decreased Abeta deposition and remained Abeta in the conditioned medium suggesting the effect of CC-EW and CCB on promoting Abeta 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. - 中文關鍵字: --
- 英文關鍵字: Neuroinflammation, Cudrania cochinchinensis, Microglia, Mixed glial culture, Amyloid β, Alzheimer’s disease