期刊
NEUROSCIENCE LETTERS
卷 483, 期 1, 页码 78-82出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2010.07.067
关键词
(-)Clausenamide; beta-amyloid; Alzheimer's disease; Apoptosis
资金
- National Natural Science Foundation of China [30801527, 30973887, U832008]
- Doctoral Program of Higher Education [20070023075]
- National Key Sci-Tech Major Special Item [2008ZX09101, 2009ZX09303-003]
The neurotoxicity of aggregated beta-amyloid (A beta) has been implicated as a critical cause in the pathogenesis of Alzheimer's disease (AD). In the present study, we investigated the effect of (-)clausenamide ((-)Clau), an aqueous extract of leaves of Clausena lassium (lour) skeel, on the neurotoxicity of A beta(25-35). The viability of differentiated PC12 cells was determined by MTT assay. Apoptosis was detected by flow cytometry. DCFH-DA was used for assessment of intracellular ROS generation, JC-1 and Rhodamine 123 for measurement of mitochondrial transmembrane potential (MMP). The intracellular calcium was determined with Fluo-3. The phosphorylation of p38 MAPK and the expression of Bcl-2, Bax, P53, Caspase 3 were examined by Western blot. The results showed that (-)Clau significantly elevated cell viability. Furthermore, (-)Clau arrested the apoptotic cascade by reversing overload of calcium, preventing ROS generation, moderated the dissipation of MMP and the misbalance of Bcl-2 and Bax, inhibiting the activation of p38 MAPK and the expression of P53 and cleaved Caspase 3. Our results suggested that (-)Clau may be a therapeutic agent for AD. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
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