Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/20126
Title: Caffeic acid phenethyl ester and its related compounds limit the functional alterations of the isolated mouse brain and liver mitochondria submitted to in vitro anoxia-reoxygenation : relationship to their antioxidant activities
Authors: Feng, Y
Lu, YW
Xu, PH
Long, Y
Wu, WM
Li, W
Wang, R
Keywords: Anoxia-reoxygenation
Caffeic acid phenethyl ester (CAPE)
Mitochondria
Phenolic compounds
Issue Date: 2008
Publisher: Elsevier
Source: Biochimica et biophysica acta, 2008, v. 1780, no. 4, p. 659-672 How to cite?
Journal: Biochimica et biophysica acta 
Abstract: It is an important therapeutic strategy to protect mitochondria from oxidative stress, especially during ischemia-reperfusion. In the present study, an attempt has been made to evaluate the protective effects of caffeic acid phenethyl ester (CAPE) and its related phenolic compounds on mouse brain and liver mitochondria injury induced by in vitro anoxia-reoxygenation. Added before anoxia or reoxygenation, CAPE markedly protected coupled respiration with the decrease in state 4 and the increases in state 3, respiratory control ratio (RCR) and ADP/O ratio in a concentration-dependent manner. CAPE effectively protected mitochondria by inhibiting the mitochondrial membranes fluidity decrease, the lipoperoxidation and the protein carbonylation increase, which indicated its protective action against the mitochondrial oxidative damage. Meanwhile, CAPE blocked the enhanced release of cardiolipin (CL) and cytochrome c (Cyt c). The related phenolic compounds like caffeic acid (CA), ferulic acid (FA) and ethyl ferulate (EF) also had different-degree protective effects. CAPE and CA were more potent than FA and EF. Their structural differences played the key role in their activity levels. These results suggest that CAPE and its related phenolic compounds protect mitochondria mainly correlated to their antioxidative activities and may be of interest for the prevention and therapy of ischemia-reperfusion injuries.
URI: http://hdl.handle.net/10397/20126
ISSN: 0006-3002
DOI: 10.1016/j.bbagen.2008.01.002
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