Abstract：
:Acrolein-induced oxidative stress is hypothesized to involve in the etiology of Alzheimer's disease (AD). Caffeic acid (CA) and caffeic acid phenethyl ester (CAPE) have antioxidative and neuroprotective properties. The present study investigated the protective effects of CA/CAPE on acrolein-induced oxidative neuronal toxicity. HT22 mouse hippocampal cells were pretreated with CA/CAPE and then exposed to acrolein. Cell viability, intracellular reactive oxygen species (ROS), and glutathione (GSH) level were measured. MAPKs and Akt/GSK3β signaling proteins as well as α/β-secretase of amyloid protein precursor were assayed by Western blotting. Pretreatment with CA/CAPE significantly attenuated acrolein-induced neurotoxicity, ROS accumulation, and GSH depletion. Further study suggested that CA/CAPE showed protective effects against acrolein by modulating MAPKs and Akt/GSK3β signaling pathways. Moreover, CA/CAPE restored the changes of β-secretase (BACE-1) and/or activation of α-secretase (ADAM-10) induced by acrolein. These findings suggest that CA/CAPE may provide a promising approach for the treatment of acrolein-related neurodegenerative diseases, such as AD.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Huang Y,Jin M,Pi R,Zhang J,Chen M,Ouyang Y,Liu A,Chao X,Liu P,Liu J,Ramassamy C,Qin Jdoi
10.1016/j.neulet.2012.12.051subject
Has Abstractpub_date
2013-02-22 00:00:00pages
146-51eissn
0304-3940issn
1872-7972pii
S0304-3940(13)00011-6journal_volume
535pub_type
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