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Beta-asarone attenuates ischemia-reperfusion-induced autophagy in rat brains via modulating JNK, p-JNK, Bcl-2 and Beclin 1.

Abstract

Beta-asarone has significant pharmacological effects on the central nervous system. It can attenuate neuronal apoptosis, but its effects on the brain ischemia-reperfusion-induced autophagy have not been reported yet. Our study was a two-stage procedure: evaluation of β-asarone effects on the autophagy at first, and then analysis of the possible mechanism. The middle cerebral artery occlusion (MCAO) model was adopted to make the brain injure and Beclin 1 was used to evaluate the autophagy. We hypothesized that the mechanism might be related to c-Jun N-terminal kinases (JNK), phospho-JNK (p-JNK), Bcl-2 and Beclin 1. To test this hypothesis, we evaluated JNK, p-JNK, Bcl-2 and Beclin 1 levels with flow cytometry. Additionally, we divided the brain into three regions: ischemic region, ischemic penumbra, and normal region, and analyzed them respectively. We found, compared to both groups II (model control) and III (low dose), Beclin 1 levels in groups IV (medium dose) and V (high dose) were significantly decreased. Beclin 1, JNK and p-JNK levels in groups VII (β-asarone) and VIII (JNK inhibitor) were significantly decreased, but Bcl-2 levels were significantly increased. Additionally, Beclin 1, JNK, p-JNK and Bcl-2 levels among the three regions had no significant differences. We conclude that β-asarone can attenuate the autophagy in a dose-dependent manner. The mechanism is likely that β-asarone can decrease JNK and p-JNK levels at first, and then increase Bcl-2 level, finally interfere with the functions of Beclin 1 during the execution of autophagy. Additionally, β-asarone can attenuate autophagy in a widespread manner.

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  • Authors+Show Affiliations

    ,

    The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou 510405, PR China.

    , , , ,

    Source

    European journal of pharmacology 680:1-3 2012 Apr 05 pg 34-40

    MeSH

    Animals
    Anisoles
    Apoptosis
    Apoptosis Regulatory Proteins
    Autophagy
    Beclin-1
    Brain
    Brain Ischemia
    Infarction, Middle Cerebral Artery
    JNK Mitogen-Activated Protein Kinases
    Middle Cerebral Artery
    Phosphopyruvate Hydratase
    Phosphorylation
    Proto-Oncogene Proteins c-bcl-2
    Rats
    Rats, Sprague-Dawley
    Reperfusion Injury

    Pub Type(s)

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

    Language

    eng

    PubMed ID

    22306244

    Citation

    Liu, Lin, et al. "Beta-asarone Attenuates Ischemia-reperfusion-induced Autophagy in Rat Brains Via Modulating JNK, p-JNK, Bcl-2 and Beclin 1." European Journal of Pharmacology, vol. 680, no. 1-3, 2012, pp. 34-40.
    Liu L, Fang YQ, Xue ZF, et al. Beta-asarone attenuates ischemia-reperfusion-induced autophagy in rat brains via modulating JNK, p-JNK, Bcl-2 and Beclin 1. Eur J Pharmacol. 2012;680(1-3):34-40.
    Liu, L., Fang, Y. Q., Xue, Z. F., He, Y. P., Fang, R. M., & Li, L. (2012). Beta-asarone attenuates ischemia-reperfusion-induced autophagy in rat brains via modulating JNK, p-JNK, Bcl-2 and Beclin 1. European Journal of Pharmacology, 680(1-3), pp. 34-40. doi:10.1016/j.ejphar.2012.01.016.
    Liu L, et al. Beta-asarone Attenuates Ischemia-reperfusion-induced Autophagy in Rat Brains Via Modulating JNK, p-JNK, Bcl-2 and Beclin 1. Eur J Pharmacol. 2012 Apr 5;680(1-3):34-40. PubMed PMID: 22306244.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Beta-asarone attenuates ischemia-reperfusion-induced autophagy in rat brains via modulating JNK, p-JNK, Bcl-2 and Beclin 1. AU - Liu,Lin, AU - Fang,Yong-Qi, AU - Xue,Zhong-Feng, AU - He,Yu-Ping, AU - Fang,Ruo-Ming, AU - Li,Ling, Y1 - 2012/01/28/ PY - 2011/09/20/received PY - 2012/01/10/revised PY - 2012/01/13/accepted PY - 2012/2/7/entrez PY - 2012/2/7/pubmed PY - 2012/9/14/medline SP - 34 EP - 40 JF - European journal of pharmacology JO - Eur. J. Pharmacol. VL - 680 IS - 1-3 N2 - Beta-asarone has significant pharmacological effects on the central nervous system. It can attenuate neuronal apoptosis, but its effects on the brain ischemia-reperfusion-induced autophagy have not been reported yet. Our study was a two-stage procedure: evaluation of β-asarone effects on the autophagy at first, and then analysis of the possible mechanism. The middle cerebral artery occlusion (MCAO) model was adopted to make the brain injure and Beclin 1 was used to evaluate the autophagy. We hypothesized that the mechanism might be related to c-Jun N-terminal kinases (JNK), phospho-JNK (p-JNK), Bcl-2 and Beclin 1. To test this hypothesis, we evaluated JNK, p-JNK, Bcl-2 and Beclin 1 levels with flow cytometry. Additionally, we divided the brain into three regions: ischemic region, ischemic penumbra, and normal region, and analyzed them respectively. We found, compared to both groups II (model control) and III (low dose), Beclin 1 levels in groups IV (medium dose) and V (high dose) were significantly decreased. Beclin 1, JNK and p-JNK levels in groups VII (β-asarone) and VIII (JNK inhibitor) were significantly decreased, but Bcl-2 levels were significantly increased. Additionally, Beclin 1, JNK, p-JNK and Bcl-2 levels among the three regions had no significant differences. We conclude that β-asarone can attenuate the autophagy in a dose-dependent manner. The mechanism is likely that β-asarone can decrease JNK and p-JNK levels at first, and then increase Bcl-2 level, finally interfere with the functions of Beclin 1 during the execution of autophagy. Additionally, β-asarone can attenuate autophagy in a widespread manner. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/22306244/Beta_asarone_attenuates_ischemia_reperfusion_induced_autophagy_in_rat_brains_via_modulating_JNK_p_JNK_Bcl_2_and_Beclin_1_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(12)00067-2 DB - PRIME DP - Unbound Medicine ER -