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Beta-asarone attenuates neuronal apoptosis induced by Beta amyloid in rat hippocampus.

Abstract

Neurodegenerative disorders, such as Alzheimer's disease (AD), is associated with the loss of neuronal cells, and it has been suggested that apoptosis is a crucial pathway in neuronal loss in AD patients. Recent evidence suggests that amyloid beta peptide (Abeta) induces neuronal apoptosis in the brain and in primary neuronal cultures. In this study, we investigated the impact of beta-asarone against the apoptosis induced by Abeta in rat hippocampus. The results showed that intrahippocampal injections of Abeta (1-42) caused apoptosis in rat hippocampus. Oral administration of beta-asarone (12.5, 25, or 50 mg/kg) for 28 d reverse the increase in the number of terminal deoxynucleotidyl transferase dUTP nick-end labeling positive cells in the hippocampus tissue. Mitochondrial dysfunction is a hallmark of beta-amyloid (Abeta)-induced neuronal toxicity in AD. Therefore, we investigated nuclear translocation of apoptosis induction factors. Our results showed that beta-asarone afforded a beneficial inhibition on both mRNA and protein expression of Bad, Bax, and cleavage of caspases 9 in rat hippocampus following intrahippocampal injections of Abeta (1-42). Our further investigation revealed that ASK1, p-MKK7, and p-c-Jun were significantly decreased after beta-asarone treatment, implicating that the modulation of ASK1/c-JNK-mediated intracellular signaling cascades might be involved in therapeutic effect of beta-asarone against Abeta toxicity. Taken together, these results suggest that beta-asarone may be a potential candidate for development as a therapeutic agent for AD.

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  • Authors+Show Affiliations

    ,

    The Institute of Medicine, Qiqihar Medical University, China.

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    Source

    MeSH

    Administration, Oral
    Alzheimer Disease
    Amyloid beta-Peptides
    Animals
    Anisoles
    Apoptosis
    Caspase 9
    DNA Nucleotidylexotransferase
    Drug Design
    Hippocampus
    JNK Mitogen-Activated Protein Kinases
    MAP Kinase Kinase Kinase 5
    Male
    Neurons
    Peptide Fragments
    Rats
    Rats, Sprague-Dawley
    Signal Transduction
    bcl-2-Associated X Protein
    bcl-Associated Death Protein

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    20460873

    Citation

    Liu, Jicheng, et al. "Beta-asarone Attenuates Neuronal Apoptosis Induced By Beta Amyloid in Rat Hippocampus." Yakugaku Zasshi : Journal of the Pharmaceutical Society of Japan, vol. 130, no. 5, 2010, pp. 737-46.
    Liu J, Li C, Xing G, et al. Beta-asarone attenuates neuronal apoptosis induced by Beta amyloid in rat hippocampus. Yakugaku Zasshi. 2010;130(5):737-46.
    Liu, J., Li, C., Xing, G., Zhou, L., Dong, M., Geng, Y., ... Niu, Y. (2010). Beta-asarone attenuates neuronal apoptosis induced by Beta amyloid in rat hippocampus. Yakugaku Zasshi : Journal of the Pharmaceutical Society of Japan, 130(5), pp. 737-46.
    Liu J, et al. Beta-asarone Attenuates Neuronal Apoptosis Induced By Beta Amyloid in Rat Hippocampus. Yakugaku Zasshi. 2010;130(5):737-46. PubMed PMID: 20460873.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Beta-asarone attenuates neuronal apoptosis induced by Beta amyloid in rat hippocampus. AU - Liu,Jicheng, AU - Li,Chengchong, AU - Xing,Guihua, AU - Zhou,Li, AU - Dong,Miaoxian, AU - Geng,Yutao, AU - Li,Xueyan, AU - Li,Jiaming, AU - Wang,Gang, AU - Zou,Dejia, AU - Niu,Yingcai, PY - 2010/5/13/entrez PY - 2010/5/13/pubmed PY - 2010/7/2/medline SP - 737 EP - 46 JF - Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan JO - Yakugaku Zasshi VL - 130 IS - 5 N2 - Neurodegenerative disorders, such as Alzheimer's disease (AD), is associated with the loss of neuronal cells, and it has been suggested that apoptosis is a crucial pathway in neuronal loss in AD patients. Recent evidence suggests that amyloid beta peptide (Abeta) induces neuronal apoptosis in the brain and in primary neuronal cultures. In this study, we investigated the impact of beta-asarone against the apoptosis induced by Abeta in rat hippocampus. The results showed that intrahippocampal injections of Abeta (1-42) caused apoptosis in rat hippocampus. Oral administration of beta-asarone (12.5, 25, or 50 mg/kg) for 28 d reverse the increase in the number of terminal deoxynucleotidyl transferase dUTP nick-end labeling positive cells in the hippocampus tissue. Mitochondrial dysfunction is a hallmark of beta-amyloid (Abeta)-induced neuronal toxicity in AD. Therefore, we investigated nuclear translocation of apoptosis induction factors. Our results showed that beta-asarone afforded a beneficial inhibition on both mRNA and protein expression of Bad, Bax, and cleavage of caspases 9 in rat hippocampus following intrahippocampal injections of Abeta (1-42). Our further investigation revealed that ASK1, p-MKK7, and p-c-Jun were significantly decreased after beta-asarone treatment, implicating that the modulation of ASK1/c-JNK-mediated intracellular signaling cascades might be involved in therapeutic effect of beta-asarone against Abeta toxicity. Taken together, these results suggest that beta-asarone may be a potential candidate for development as a therapeutic agent for AD. SN - 0031-6903 UR - https://www.unboundmedicine.com/medline/citation/20460873/Beta_asarone_attenuates_neuronal_apoptosis_induced_by_Beta_amyloid_in_rat_hippocampus_ L2 - http://joi.jlc.jst.go.jp/JST.JSTAGE/yakushi/130.737?from=PubMed&lang=en DB - PRIME DP - Unbound Medicine ER -