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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):34-40EJ

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.

Authors+Show Affiliations

The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou 510405, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

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 -