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Beta-asarone protection against beta-amyloid-induced neurotoxicity in PC12 cells via JNK signaling and modulation of Bcl-2 family proteins.

Abstract

Neurodegenerative brain disorders such as Alzheimer's disease have been well investigated. However, significant methods for the treatment of the promotion and progression of Alzheimer's disease are unavailable to date. Apoptosis is a crucial pathway in neuronal loss in Alzheimer's disease patients. Thus, the suppression of apoptosis may be an effective therapeutic strategy for Alzheimer's disease. In this study, we evaluated the effect of beta-asarone on beta-amyloid (Abeta)-induced toxicity in cultured PC12 cells. Our data show significant induction of apoptosis in PC12 cells incubated with Abeta peptide, and this effect was reduced by beta-asarone. Beta-asarone reduced Abeta-induced JNK activation. In addition, beta-asarone attenuates Abeta-induced down-regulation of Bcl-w and Bcl-xL in a JNK-dependent manner, and subsequent inhibition mitochondrial release of cytochrome c and activation of caspase-3. Together, these findings indicate that Abeta-induced apoptosis of PC12 cells proceeds through mitochondrial pathway. Further, the JNK signaling cascade plays a role in regulating the anti-apoptotic effects of beta-asarone. Thus, our results indicate that beta-asarone might be a potentially therapeutic compound for Alzheimer's disease.

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  • Authors+Show Affiliations

    ,

    The Institute of Medicine, Qiqihar Medical University, Qiqihar, China.

    , , , , , , , ,

    Source

    European journal of pharmacology 635:1-3 2010 Jun 10 pg 96-102

    MeSH

    Amyloid beta-Peptides
    Animals
    Anisoles
    Apoptosis
    Cytochromes c
    Gene Expression Regulation
    JNK Mitogen-Activated Protein Kinases
    MAP Kinase Signaling System
    Neurotoxins
    PC12 Cells
    Phosphorylation
    Proto-Oncogene Proteins c-bcl-2
    Rats
    bcl-X Protein

    Pub Type(s)

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

    Language

    eng

    PubMed ID

    20307525

    Citation

    Li, Chengchong, et al. "Beta-asarone Protection Against Beta-amyloid-induced Neurotoxicity in PC12 Cells Via JNK Signaling and Modulation of Bcl-2 Family Proteins." European Journal of Pharmacology, vol. 635, no. 1-3, 2010, pp. 96-102.
    Li C, Xing G, Dong M, et al. Beta-asarone protection against beta-amyloid-induced neurotoxicity in PC12 cells via JNK signaling and modulation of Bcl-2 family proteins. Eur J Pharmacol. 2010;635(1-3):96-102.
    Li, C., Xing, G., Dong, M., Zhou, L., Li, J., Wang, G., ... Niu, Y. (2010). Beta-asarone protection against beta-amyloid-induced neurotoxicity in PC12 cells via JNK signaling and modulation of Bcl-2 family proteins. European Journal of Pharmacology, 635(1-3), pp. 96-102. doi:10.1016/j.ejphar.2010.03.013.
    Li C, et al. Beta-asarone Protection Against Beta-amyloid-induced Neurotoxicity in PC12 Cells Via JNK Signaling and Modulation of Bcl-2 Family Proteins. Eur J Pharmacol. 2010 Jun 10;635(1-3):96-102. PubMed PMID: 20307525.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Beta-asarone protection against beta-amyloid-induced neurotoxicity in PC12 cells via JNK signaling and modulation of Bcl-2 family proteins. AU - Li,Chengchong, AU - Xing,Guihua, AU - Dong,Miaoxian, AU - Zhou,Li, AU - Li,Jiaming, AU - Wang,Gang, AU - Zou,Dejia, AU - Wang,Rui, AU - Liu,Jicheng, AU - Niu,Yingcai, Y1 - 2010/03/20/ PY - 2009/12/11/received PY - 2010/02/15/revised PY - 2010/03/03/accepted PY - 2010/3/24/entrez PY - 2010/3/24/pubmed PY - 2010/8/18/medline SP - 96 EP - 102 JF - European journal of pharmacology JO - Eur. J. Pharmacol. VL - 635 IS - 1-3 N2 - Neurodegenerative brain disorders such as Alzheimer's disease have been well investigated. However, significant methods for the treatment of the promotion and progression of Alzheimer's disease are unavailable to date. Apoptosis is a crucial pathway in neuronal loss in Alzheimer's disease patients. Thus, the suppression of apoptosis may be an effective therapeutic strategy for Alzheimer's disease. In this study, we evaluated the effect of beta-asarone on beta-amyloid (Abeta)-induced toxicity in cultured PC12 cells. Our data show significant induction of apoptosis in PC12 cells incubated with Abeta peptide, and this effect was reduced by beta-asarone. Beta-asarone reduced Abeta-induced JNK activation. In addition, beta-asarone attenuates Abeta-induced down-regulation of Bcl-w and Bcl-xL in a JNK-dependent manner, and subsequent inhibition mitochondrial release of cytochrome c and activation of caspase-3. Together, these findings indicate that Abeta-induced apoptosis of PC12 cells proceeds through mitochondrial pathway. Further, the JNK signaling cascade plays a role in regulating the anti-apoptotic effects of beta-asarone. Thus, our results indicate that beta-asarone might be a potentially therapeutic compound for Alzheimer's disease. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/20307525/Beta_asarone_protection_against_beta_amyloid_induced_neurotoxicity_in_PC12_cells_via_JNK_signaling_and_modulation_of_Bcl_2_family_proteins_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(10)00206-2 DB - PRIME DP - Unbound Medicine ER -