Journal
NEUROSCIENCE LETTERS
Volume 480, Issue 1, Pages 21-24Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2010.05.062
Keywords
Curcumin; Intracellular A beta; Prefrontal cortical neurons; Caspase-3; AKT; Neuronal protective effect
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Funding
- Ministry of Science and Technology of China [2006CB500706]
- National Science Foundation of China (NSFC) [30670658]
- Minzu University [MUC985]
- 111 project [BO8044]
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Recently the neuronal toxicity of intracellular amyloid beta (iA beta) in Alzheimer's disease is attracting more and more attention. The present study explored the effects of curcumin on the iA beta-induced toxicity in primary cultured rat prefrontal cortical neurons. The cell viability of primary cultured prefrontal cortical neurons decreased significantly after virus driven transfection of A beta from 1 day to 7 days. Interestingly, administration of 1 mu M, 10 mu M or 20 mu M of curcumin significantly inhibited the iA beta-induced toxicity in primary cultured rat prefrontal cortical neurons tested by MTT and LDH release assays. We further studied the involvements of apoptotic or neuroprotective pathway proteins in curcumin protection against iA beta-induced cytotoxicity in primary cultured rat prefrontal cortical neurons. The results demonstrated that the contents of activated caspase-3 increased significantly by iA beta, while curcumin significantly inhibited the iA beta-induced increases of activated caspase-3 tested by Western blot. And the contents of p-AKT decreased significantly after iA beta treatment, while administration of curcumin significantly inhibited the iA beta-induced decreases in the contents of p-AKT. The results suggest that curcumin may play a protective effect in primary cultured rat prefrontal cortical neurons against iA beta-induced cytotoxicity, and both AKT and caspase-3 are involved in the curcumin-induced protective effects. (C) 2010 Published by Elsevier Ireland Ltd.
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