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

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 an...

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Published inBiochimica et biophysica acta Vol. 1780; no. 4; pp. 659 - 672
Main Authors Feng, Yun, Lu, Ying-Wei, Xu, Pei-Han, Long, Yuan, Wu, Wei-Min, Li, Wei, Wang, Rui
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.04.2008
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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.
AbstractList 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.
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.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.
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.
Author Long, Yuan
Li, Wei
Lu, Ying-Wei
Wu, Wei-Min
Xu, Pei-Han
Feng, Yun
Wang, Rui
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Keywords Mitochondria
Anoxia–reoxygenation
Caffeic acid phenethyl ester (CAPE)
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Snippet It is an important therapeutic strategy to protect mitochondria from oxidative stress, especially during ischemia–reperfusion. In the present study, an attempt...
It is an important therapeutic strategy to protect mitochondria from oxidative stress, especially during ischemia-reperfusion. In the present study, an attempt...
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SubjectTerms Anaerobiosis
Animals
Anisotropy
Anoxia–reoxygenation
Antioxidants - metabolism
Brain - drug effects
Brain - metabolism
Caffeic acid phenethyl ester (CAPE)
Caffeic Acids - chemistry
Caffeic Acids - pharmacology
Coumaric Acids - chemistry
Coumaric Acids - pharmacology
Cytochromes c - secretion
Dose-Response Relationship, Drug
Male
Mice
Mitochondria
Mitochondria - drug effects
Mitochondria - metabolism
Mitochondria, Liver - drug effects
Mitochondria, Liver - metabolism
Mitochondrial Membranes - chemistry
Mitochondrial Membranes - drug effects
Mitochondrial Membranes - metabolism
Molecular Structure
Oxygen - pharmacology
Phenolic compounds
Phenylethyl Alcohol - analogs & derivatives
Phenylethyl Alcohol - chemistry
Phenylethyl Alcohol - pharmacology
Thiobarbituric Acid Reactive Substances - metabolism
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
URI https://dx.doi.org/10.1016/j.bbagen.2008.01.002
https://www.ncbi.nlm.nih.gov/pubmed/18230365
https://www.proquest.com/docview/70438428
Volume 1780
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