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Ferulic acid ethyl ester protects neurons against amyloid beta- peptide(1-42)-induced oxidative stress and neurotoxicity: relationship to antioxidant activity.
J Neurochem. 2005 Feb; 92(4):749-58.JN

Abstract

Alzheimer's disease (AD) is neuropathologically characterized by depositions of extracellular amyloid and intracellular neurofibrillary tangles, associated with loss of neurons in the brain. Amyloid beta-peptide (Abeta) is the major component of senile plaques and is considered to have a causal role in the development and progress of AD. Several lines of evidence suggest that enhanced oxidative stress and inflammation play important roles in the pathogenesis or progression of AD. The present study aimed to investigate the protective effects of ethyl-4-hydroxy-3-methoxycinnamic acid (FAEE), a phenolic compound which shows antioxidant and anti-inflammatory activity, on Abeta(1-42)-induced oxidative stress and neurotoxicity. We hypothesized that the structure of FAEE would facilitate radical scavenging and may induce protective proteins. Abeta(1-42) decreases cell viability, which was correlated with increased free radical formation, protein oxidation (protein carbonyl, 3-nitrotyrosine), lipid peroxidation (4-hydroxy-2-trans-nonenal) and inducible nitric oxide synthase. Pre-treatment of primary hippocampal cultures with FAEE significantly attenuated Abeta(1-42)-induced cytotoxicity, intracellular reactive oxygen species accumulation, protein oxidation, lipid peroxidation and induction of inducible nitric oxide synthase. Treatment of neurons with Abeta(1-42) increases levels of heme oxygenase-1 and heat shock protein 72. Consistent with a cellular stress response to the Abeta(1-42)-induced oxidative stress, FAEE treatment increases the levels of heme oxygenase-1 and heat shock protein 72, which may be regulated by oxidative stresses in a coordinated manner and play a pivotal role in the cytoprotection of neuronal cells against Abeta(1-42)-induced toxicity. These results suggest that FAEE exerts protective effects against Abeta(1-42) toxicity by modulating oxidative stress directly and by inducing protective genes. These findings suggest that FAEE could potentially be of importance for the treatment of AD and other oxidative stress-related diseases.

Authors+Show Affiliations

Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15686476

Citation

Sultana, Rukhsana, et al. "Ferulic Acid Ethyl Ester Protects Neurons Against Amyloid Beta- Peptide(1-42)-induced Oxidative Stress and Neurotoxicity: Relationship to Antioxidant Activity." Journal of Neurochemistry, vol. 92, no. 4, 2005, pp. 749-58.
Sultana R, Ravagna A, Mohmmad-Abdul H, et al. Ferulic acid ethyl ester protects neurons against amyloid beta- peptide(1-42)-induced oxidative stress and neurotoxicity: relationship to antioxidant activity. J Neurochem. 2005;92(4):749-58.
Sultana, R., Ravagna, A., Mohmmad-Abdul, H., Calabrese, V., & Butterfield, D. A. (2005). Ferulic acid ethyl ester protects neurons against amyloid beta- peptide(1-42)-induced oxidative stress and neurotoxicity: relationship to antioxidant activity. Journal of Neurochemistry, 92(4), 749-58.
Sultana R, et al. Ferulic Acid Ethyl Ester Protects Neurons Against Amyloid Beta- Peptide(1-42)-induced Oxidative Stress and Neurotoxicity: Relationship to Antioxidant Activity. J Neurochem. 2005;92(4):749-58. PubMed PMID: 15686476.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ferulic acid ethyl ester protects neurons against amyloid beta- peptide(1-42)-induced oxidative stress and neurotoxicity: relationship to antioxidant activity. AU - Sultana,Rukhsana, AU - Ravagna,Agrippino, AU - Mohmmad-Abdul,Hafiz, AU - Calabrese,Vittorio, AU - Butterfield,D Allan, PY - 2005/2/3/pubmed PY - 2005/3/22/medline PY - 2005/2/3/entrez SP - 749 EP - 58 JF - Journal of neurochemistry JO - J Neurochem VL - 92 IS - 4 N2 - Alzheimer's disease (AD) is neuropathologically characterized by depositions of extracellular amyloid and intracellular neurofibrillary tangles, associated with loss of neurons in the brain. Amyloid beta-peptide (Abeta) is the major component of senile plaques and is considered to have a causal role in the development and progress of AD. Several lines of evidence suggest that enhanced oxidative stress and inflammation play important roles in the pathogenesis or progression of AD. The present study aimed to investigate the protective effects of ethyl-4-hydroxy-3-methoxycinnamic acid (FAEE), a phenolic compound which shows antioxidant and anti-inflammatory activity, on Abeta(1-42)-induced oxidative stress and neurotoxicity. We hypothesized that the structure of FAEE would facilitate radical scavenging and may induce protective proteins. Abeta(1-42) decreases cell viability, which was correlated with increased free radical formation, protein oxidation (protein carbonyl, 3-nitrotyrosine), lipid peroxidation (4-hydroxy-2-trans-nonenal) and inducible nitric oxide synthase. Pre-treatment of primary hippocampal cultures with FAEE significantly attenuated Abeta(1-42)-induced cytotoxicity, intracellular reactive oxygen species accumulation, protein oxidation, lipid peroxidation and induction of inducible nitric oxide synthase. Treatment of neurons with Abeta(1-42) increases levels of heme oxygenase-1 and heat shock protein 72. Consistent with a cellular stress response to the Abeta(1-42)-induced oxidative stress, FAEE treatment increases the levels of heme oxygenase-1 and heat shock protein 72, which may be regulated by oxidative stresses in a coordinated manner and play a pivotal role in the cytoprotection of neuronal cells against Abeta(1-42)-induced toxicity. These results suggest that FAEE exerts protective effects against Abeta(1-42) toxicity by modulating oxidative stress directly and by inducing protective genes. These findings suggest that FAEE could potentially be of importance for the treatment of AD and other oxidative stress-related diseases. SN - 0022-3042 UR - https://www.unboundmedicine.com/medline/citation/15686476/Ferulic_acid_ethyl_ester_protects_neurons_against_amyloid_beta__peptide_1_42__induced_oxidative_stress_and_neurotoxicity:_relationship_to_antioxidant_activity_ L2 - https://doi.org/10.1111/j.1471-4159.2004.02899.x DB - PRIME DP - Unbound Medicine ER -