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Protective effects of caffeic acid and caffeic acid phenethyl ester against acrolein-induced neurotoxicity in HT22 mouse hippocampal cells

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Title: Protective effects of caffeic acid and caffeic acid phenethyl ester against acrolein-induced neurotoxicity in HT22 mouse hippocampal cells
Authors: Huang, Ying, Jin, Minghua, Pi, Rongbiao, Zhang, Jun, Chen, Meihui, Ouyang, Ying, Liu, Anmin, Chao, Xiaojuan, Liu, Peiqing, Liu, Jun, Ramassamy, Charles, Qin, Jian
Contributors: Sun Yat-sen University Guangzhou (SYSU), Armand-Frappier Santé Biotechnologie Research Centre (INRS-AFSB), Institut National de la Recherche Scientifique Québec (INRS)-Pasteur Network (Réseau International des Instituts Pasteur), This study was supported by Fundamental Research Funds for the Central Universities (No. 10ykpy23) and Guangdong Provincial International Cooperation Project of Science & Technology (No. 2012B050300015) to R. Pi and National Natural Science Foundation of China (No. 30371717) to J Qin.
Source: ISSN: 0304-3940.
Publisher Information: CCSD
Elsevier
Publication Year: 2013
Collection: Réseau International des Instituts Pasteur, Paris: HAL-RIIP
Subject Terms: Oxidative stress, Alzheimer's disease, Acrolein, Caffeic acid, MESH: ADAM Proteins/mCetabolismCell Line, MESH: Acrolein/toxicity, MESH: Glycogen Synthase Kinase 3/metabolism, MESH: Hippocampus/cytology, MESH: Hippocampus/drug effects, MESH: MAP Kinase Signaling System/drug effects, MESH: Membrane Proteins/metabolism, MESH: Mice, MESH: Neurons/cytology, MESH: Neurons/drug effects, MESH: Neuroprotective Agents/pharmacology, MESH: Oxidative Stress, MESH: Amyloid Precursor Protein, MESH: Phenylethyl Alcohol/analogs & derivatives, MESH: Proto-Oncogene Proteins c-akt/metabolism, MESH: Reactive Oxygen Species/metabolism, MESH: Secretases/metabolism, MESH: Animals, MESH: Antioxidants/pharmacology, MESH: Aspartic Acid Endopeptidases/metabolism, MESH: Caffeic Acids/pharmacology, MESH: Cell Survival/drug effects, MESH: Glutathione/metabolism, [SDV]Life Sciences [q-bio], [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology
Description: International audience ; 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.
Document Type: article in journal/newspaper
Language: English
Relation: info:eu-repo/semantics/altIdentifier/pmid/23313590; PUBMED: 23313590
DOI: 10.1016/j.neulet.2012.12.051
Availability: https://riip.hal.science/pasteur-01131056
https://doi.org/10.1016/j.neulet.2012.12.051
Accession Number: edsbas.76190D1D
Database: BASE
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PubType: Academic Journal
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  Label: Title
  Group: Ti
  Data: Protective effects of caffeic acid and caffeic acid phenethyl ester against acrolein-induced neurotoxicity in HT22 mouse hippocampal cells
– Name: Author
  Label: Authors
  Group: Au
  Data: <searchLink fieldCode="AR" term="%22Huang%2C+Ying%22">Huang, Ying</searchLink><br /><searchLink fieldCode="AR" term="%22Jin%2C+Minghua%22">Jin, Minghua</searchLink><br /><searchLink fieldCode="AR" term="%22Pi%2C+Rongbiao%22">Pi, Rongbiao</searchLink><br /><searchLink fieldCode="AR" term="%22Zhang%2C+Jun%22">Zhang, Jun</searchLink><br /><searchLink fieldCode="AR" term="%22Chen%2C+Meihui%22">Chen, Meihui</searchLink><br /><searchLink fieldCode="AR" term="%22Ouyang%2C+Ying%22">Ouyang, Ying</searchLink><br /><searchLink fieldCode="AR" term="%22Liu%2C+Anmin%22">Liu, Anmin</searchLink><br /><searchLink fieldCode="AR" term="%22Chao%2C+Xiaojuan%22">Chao, Xiaojuan</searchLink><br /><searchLink fieldCode="AR" term="%22Liu%2C+Peiqing%22">Liu, Peiqing</searchLink><br /><searchLink fieldCode="AR" term="%22Liu%2C+Jun%22">Liu, Jun</searchLink><br /><searchLink fieldCode="AR" term="%22Ramassamy%2C+Charles%22">Ramassamy, Charles</searchLink><br /><searchLink fieldCode="AR" term="%22Qin%2C+Jian%22">Qin, Jian</searchLink>
– Name: Author
  Label: Contributors
  Group: Au
  Data: Sun Yat-sen University Guangzhou (SYSU)<br />Armand-Frappier Santé Biotechnologie Research Centre (INRS-AFSB)<br />Institut National de la Recherche Scientifique Québec (INRS)-Pasteur Network (Réseau International des Instituts Pasteur)<br />This study was supported by Fundamental Research Funds for the Central Universities (No. 10ykpy23) and Guangdong Provincial International Cooperation Project of Science & Technology (No. 2012B050300015) to R. Pi and National Natural Science Foundation of China (No. 30371717) to J Qin.
– Name: TitleSource
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  Data: <i>ISSN: 0304-3940</i>.
– Name: Publisher
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  Data: CCSD<br />Elsevier
– Name: DatePubCY
  Label: Publication Year
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  Data: 2013
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  Data: Réseau International des Instituts Pasteur, Paris: HAL-RIIP
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  Data: <searchLink fieldCode="DE" term="%22Oxidative+stress%22">Oxidative stress</searchLink><br /><searchLink fieldCode="DE" term="%22Alzheimer's+disease%22">Alzheimer's disease</searchLink><br /><searchLink fieldCode="DE" term="%22Acrolein%22">Acrolein</searchLink><br /><searchLink fieldCode="DE" term="%22Caffeic+acid%22">Caffeic acid</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+ADAM+Proteins%2FmCetabolismCell+Line%22">MESH: ADAM Proteins/mCetabolismCell Line</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Acrolein%2Ftoxicity%22">MESH: Acrolein/toxicity</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Glycogen+Synthase+Kinase+3%2Fmetabolism%22">MESH: Glycogen Synthase Kinase 3/metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Hippocampus%2Fcytology%22">MESH: Hippocampus/cytology</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Hippocampus%2Fdrug+effects%22">MESH: Hippocampus/drug effects</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+MAP+Kinase+Signaling+System%2Fdrug+effects%22">MESH: MAP Kinase Signaling System/drug effects</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Membrane+Proteins%2Fmetabolism%22">MESH: Membrane Proteins/metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Mice%22">MESH: Mice</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Neurons%2Fcytology%22">MESH: Neurons/cytology</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Neurons%2Fdrug+effects%22">MESH: Neurons/drug effects</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Neuroprotective+Agents%2Fpharmacology%22">MESH: Neuroprotective Agents/pharmacology</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Oxidative+Stress%22">MESH: Oxidative Stress</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Amyloid+Precursor+Protein%22">MESH: Amyloid Precursor Protein</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Phenylethyl+Alcohol%2Fanalogs+%26+derivatives%22">MESH: Phenylethyl Alcohol/analogs & derivatives</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Proto-Oncogene+Proteins+c-akt%2Fmetabolism%22">MESH: Proto-Oncogene Proteins c-akt/metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Reactive+Oxygen+Species%2Fmetabolism%22">MESH: Reactive Oxygen Species/metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Secretases%2Fmetabolism%22">MESH: Secretases/metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Animals%22">MESH: Animals</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Antioxidants%2Fpharmacology%22">MESH: Antioxidants/pharmacology</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Aspartic+Acid+Endopeptidases%2Fmetabolism%22">MESH: Aspartic Acid Endopeptidases/metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Caffeic+Acids%2Fpharmacology%22">MESH: Caffeic Acids/pharmacology</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Cell+Survival%2Fdrug+effects%22">MESH: Cell Survival/drug effects</searchLink><br /><searchLink fieldCode="DE" term="%22MESH%3A+Glutathione%2Fmetabolism%22">MESH: Glutathione/metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22[SDV]Life+Sciences+[q-bio]%22">[SDV]Life Sciences [q-bio]</searchLink><br /><searchLink fieldCode="DE" term="%22[SDV%2ENEU%2ENB]Life+Sciences+[q-bio]%2FNeurons+and+Cognition+[q-bio%2ENC]%2FNeurobiology%22">[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology</searchLink>
– Name: Abstract
  Label: Description
  Group: Ab
  Data: International audience ; 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.
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  Data: info:eu-repo/semantics/altIdentifier/pmid/23313590; PUBMED: 23313590
– Name: DOI
  Label: DOI
  Group: ID
  Data: 10.1016/j.neulet.2012.12.051
– Name: URL
  Label: Availability
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  Data: https://riip.hal.science/pasteur-01131056<br />https://doi.org/10.1016/j.neulet.2012.12.051
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  Data: edsbas.76190D1D
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      – Type: doi
        Value: 10.1016/j.neulet.2012.12.051
    Languages:
      – Text: English
    Subjects:
      – SubjectFull: Oxidative stress
        Type: general
      – SubjectFull: Alzheimer's disease
        Type: general
      – SubjectFull: Acrolein
        Type: general
      – SubjectFull: Caffeic acid
        Type: general
      – SubjectFull: MESH: ADAM Proteins/mCetabolismCell Line
        Type: general
      – SubjectFull: MESH: Acrolein/toxicity
        Type: general
      – SubjectFull: MESH: Glycogen Synthase Kinase 3/metabolism
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      – SubjectFull: MESH: MAP Kinase Signaling System/drug effects
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      – SubjectFull: MESH: Membrane Proteins/metabolism
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      – SubjectFull: MESH: Neurons/drug effects
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      – SubjectFull: MESH: Amyloid Precursor Protein
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      – SubjectFull: MESH: Cell Survival/drug effects
        Type: general
      – SubjectFull: MESH: Glutathione/metabolism
        Type: general
      – SubjectFull: [SDV]Life Sciences [q-bio]
        Type: general
      – SubjectFull: [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology
        Type: general
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      – TitleFull: Protective effects of caffeic acid and caffeic acid phenethyl ester against acrolein-induced neurotoxicity in HT22 mouse hippocampal cells
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            NameFull: This study was supported by Fundamental Research Funds for the Central Universities (No. 10ykpy23) and Guangdong Provincial International Cooperation Project of Science & Technology (No. 2012B050300015) to R. Pi and National Natural Science Foundation of China (No. 30371717) to J Qin.
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