Abstract:
:Alzheimer's disease is the most common form of dementia, causing progressive cognitive dysfunction, particularly memory loss. Recently, modulation of beta-amyloid (Abeta) toxicity, one of the major potential causes of Alzheimer's disease, has emerged as a possible therapeutic approach to control the onset of Alzheimer's disease. In this study, we investigated the neuroprotective effects and possible mechanisms by which 19-hydroxy-1alpha,6-diacetoxy-6,7-seco-ent-kaur-16-en-15-one-7,20-olide (named as CBNU06), a new diterpene isolated from Isodon japonicus, acts against Abeta-induced toxicity in PC12 cells. Pretreatment with CBNU06 (20 microg/ml) prior to Abeta(25)(-35) (25 microM) significantly increased the viability of PC12 cells in a dose-dependent manner when examined by Hoechst staining, MTT assay and Trypan blue exclusion assay. This protective effect was accompanied by the decrease in translocation of NF-kappaB p50 and p65 from the cytoplasm to the nucleus, and followed by the decrease in cyclooxygenase-2 (COX-2) levels. In addition, pretreatment with CBNU06 significantly reversed the effect of Abeta on Bax and Bcl-2. Taken together, these results suggest that CBNU06 protected PC12 cells against Abeta-induced neurotoxicity through the inhibition of the NF-kappaB signaling pathways. Therefore, CBNU06 has the possible beneficial effects in Alzheimer's disease by attenuating Abeta-induced toxicity.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Kim HS,Lim JY,Sul D,Hwang BY,Won TJ,Hwang KW,Park SYdoi
10.1016/j.ejphar.2009.09.007subject
Has Abstractpub_date
2009-11-10 00:00:00pages
25-31issue
1-3eissn
0014-2999issn
1879-0712pii
S0014-2999(09)00773-0journal_volume
622pub_type
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journal_title:European journal of pharmacology
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