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Opposing needling promotes behavior recovery and exerts neuroprotection via the cAMP/PKA/CREB signal transduction pathway in transient MCAO rats.
Mol Med Rep. 2016 Mar; 13(3):2060-70.MM

Abstract

The aim of the present study was to investigate whether the cyclic adenosine 3',5'‑monophosphate (cAMP)/protein kinase A(PKA)/cAMP‑responsive element binding protein (CREB) signal transduction pathway triggered by γ‑aminobutyric acid class B (GABA(B)) receptor activation is involved in neuroprotection against ischemia and behavioral recovery induced by opposing needling (ON). A total of 80 rats were randomly divided into four groups: A sham operation group, an ischemia group, an ON group and an ON group effectively inhibited by the GABA(B) receptor antagonist, CGP35384 (n=20/group). The behavior of the rats was assessed by their neurological deficit score, whereas the impairment of gait was examined using the CatWalk system. The volume of cerebral infarction was examined upon treatment with 2,3,5‑triphenyltetrazolium chloride. The expression levels of CREB, GABA(B1) and GABA(B2) were examined by western blotting and reverse transcription‑quantitative polymerase chain reaction, and the activity of adenylyl cyclase (AC), cAMP and PKA in the serum was detected using an enzyme‑linked immunosorbent assay. In the present study, in comparison with other groups, the ON group exhibited a reduced score for the neurological deficit, the stride length and swing speed were improved, and the volume of infarction was reduced. However, these effects were reversed upon administration of CGP35384. Additionally, the expression levels of CREB, GABA(B1) and GABA(B2) were increased in the ON group. The levels of AC, cAMP and PKA in the serum were also increased in the ON group, whereas the addition of CGP35384 reversed these effects. The results of the present study demonstrated that ON markedly protected the brain against transient cerebral ischemic injury, and this effect was possibly mediated by the activation of the GABAB/cAMP/PKA/CREB signal transduction pathway. These findings implied that ON may be a potential therapeutic method for treating stroke.

Authors+Show Affiliations

Department of Rehabilitation Medicine, Rehabilitation Hospital, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350001, P.R. China.Department of Rehabilitation Medicine, Rehabilitation Hospital, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350001, P.R. China.College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.Department of Rehabilitation Medicine, Rehabilitation Hospital, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350001, P.R. China.College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.

Pub Type(s)

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

Language

eng

PubMed ID

26780954

Citation

Jiang, Yijing, et al. "Opposing Needling Promotes Behavior Recovery and Exerts Neuroprotection Via the cAMP/PKA/CREB Signal Transduction Pathway in Transient MCAO Rats." Molecular Medicine Reports, vol. 13, no. 3, 2016, pp. 2060-70.
Jiang Y, Yang S, Tao J, et al. Opposing needling promotes behavior recovery and exerts neuroprotection via the cAMP/PKA/CREB signal transduction pathway in transient MCAO rats. Mol Med Rep. 2016;13(3):2060-70.
Jiang, Y., Yang, S., Tao, J., Lin, Z., Ye, X., You, Y., Peng, J., Hong, Z., & Chen, L. (2016). Opposing needling promotes behavior recovery and exerts neuroprotection via the cAMP/PKA/CREB signal transduction pathway in transient MCAO rats. Molecular Medicine Reports, 13(3), 2060-70. https://doi.org/10.3892/mmr.2016.4773
Jiang Y, et al. Opposing Needling Promotes Behavior Recovery and Exerts Neuroprotection Via the cAMP/PKA/CREB Signal Transduction Pathway in Transient MCAO Rats. Mol Med Rep. 2016;13(3):2060-70. PubMed PMID: 26780954.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Opposing needling promotes behavior recovery and exerts neuroprotection via the cAMP/PKA/CREB signal transduction pathway in transient MCAO rats. AU - Jiang,Yijing, AU - Yang,Shanli, AU - Tao,Jing, AU - Lin,Zhicheng, AU - Ye,Xiaoqian, AU - You,Yongmei, AU - Peng,Jun, AU - Hong,Zhenfeng, AU - Chen,Lidian, Y1 - 2016/01/13/ PY - 2015/02/04/received PY - 2015/10/28/accepted PY - 2016/1/20/entrez PY - 2016/1/20/pubmed PY - 2016/12/27/medline SP - 2060 EP - 70 JF - Molecular medicine reports JO - Mol Med Rep VL - 13 IS - 3 N2 - The aim of the present study was to investigate whether the cyclic adenosine 3',5'‑monophosphate (cAMP)/protein kinase A(PKA)/cAMP‑responsive element binding protein (CREB) signal transduction pathway triggered by γ‑aminobutyric acid class B (GABA(B)) receptor activation is involved in neuroprotection against ischemia and behavioral recovery induced by opposing needling (ON). A total of 80 rats were randomly divided into four groups: A sham operation group, an ischemia group, an ON group and an ON group effectively inhibited by the GABA(B) receptor antagonist, CGP35384 (n=20/group). The behavior of the rats was assessed by their neurological deficit score, whereas the impairment of gait was examined using the CatWalk system. The volume of cerebral infarction was examined upon treatment with 2,3,5‑triphenyltetrazolium chloride. The expression levels of CREB, GABA(B1) and GABA(B2) were examined by western blotting and reverse transcription‑quantitative polymerase chain reaction, and the activity of adenylyl cyclase (AC), cAMP and PKA in the serum was detected using an enzyme‑linked immunosorbent assay. In the present study, in comparison with other groups, the ON group exhibited a reduced score for the neurological deficit, the stride length and swing speed were improved, and the volume of infarction was reduced. However, these effects were reversed upon administration of CGP35384. Additionally, the expression levels of CREB, GABA(B1) and GABA(B2) were increased in the ON group. The levels of AC, cAMP and PKA in the serum were also increased in the ON group, whereas the addition of CGP35384 reversed these effects. The results of the present study demonstrated that ON markedly protected the brain against transient cerebral ischemic injury, and this effect was possibly mediated by the activation of the GABAB/cAMP/PKA/CREB signal transduction pathway. These findings implied that ON may be a potential therapeutic method for treating stroke. SN - 1791-3004 UR - https://www.unboundmedicine.com/medline/citation/26780954/Opposing_needling_promotes_behavior_recovery_and_exerts_neuroprotection_via_the_cAMP/PKA/CREB_signal_transduction_pathway_in_transient_MCAO_rats_ L2 - http://www.spandidos-publications.com/mmr/13/3/2060 DB - PRIME DP - Unbound Medicine ER -