Electroacupuncture-like stimulation at Baihui and Dazhui acupoints exerts neuroprotective effects through activation of the brain-derived neurotrophic factor-mediated MEK1/2/ERK1/2/p90RSK/bad signaling pathway in mild transient focal cerebral ischemia in
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  • 作者：Chin Yi Cheng (7) (7)
    Jaung Geng Lin (7)
    Shan Yu Su (7) (7)
    Nou Ying Tang (7)
    Shung Te Kao (7)
    Ching Liang Hsieh (7) (7) (7)
  • 关键词：Electroacupuncture ; Brain ; derived neurotrophic factor ; Phospho ; ERK1/2 ; Phospho ; p90RSK ; Phospho ; Bad ; Apoptosis
  • 刊名：BMC Complementary and Alternative Medicine
  • 出版年：2014
  • 出版时间：December 2014
  • 年：2014
  • 卷：14
  • 期：1
  • 全文大小：2,654 KB
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    41. The pre-publication history for this paper can be accessed here: http://www.biomedcentral.com/1472-6882/14/92/prepub
  • 作者单位：Chin Yi Cheng (7) (7)
    Jaung Geng Lin (7)
    Shan Yu Su (7) (7)
    Nou Ying Tang (7)
    Shung Te Kao (7)
    Ching Liang Hsieh (7) (7) (7)

    7. Graduate Institute of Integrated Medicine, College of Chinese Medicine, China Medical University, Taichung, 40402, Taiwan
  • ISSN：1472-6882
文摘
Background This study was designed to evaluate the effects of electroacupuncture-like stimulation at Baihui (GV20) and Dazhui (GV14) acupoints (EA at acupoints) following mild cerebral ischemia-reperfusion (I/R) injury. Furthermore, we investigated whether brain-derived neurotrophic factor (BDNF)-mediated activation of extracellular signal-regulated kinase (ERK)1/2 signaling pathway is involved in the neuroprotection induced by EA at acupoints. Methods Rats were subjected to middle cerebral artery occlusion (MCAo) for 15?min followed by reperfusion for 3 d. EA at acupoints was applied 1 d postreperfusion then once daily for 2 consecutive days. Results Following the application of EA at acupoints, initiated 1 d postreperfusion, we observed significant reductions in the cerebral infarct area, neurological deficit scores, active caspase-3 protein expression, and apoptosis in the ischemic cortex after 3 d of reperfusion. We also observed markedly upregulated BDNF, phospho-Raf-1 (pRaf-1), phospho-MEK1/2 (pMEK1/2), phospho-ERK1/2 (pERK1/2), phospho-90?kDa ribosomal S6 kinase (pp90RSK), and phospho-Bad (pBad) expression, and restored neuronal nuclear antigen (NeuN) expression. Pretreatment with the MEK1/2 inhibitor U0126 abrogated the effects of EA at acupoints on cerebral infarct size, neurological deficits, active caspase-3 protein, and apoptosis in the ischemic cortex after 3 d of reperfusion. Pretreatment with U0126 also abrogated the effects of EA at acupoints on pMEK1/2, pERK1/2, pp90RSK, pBad, and NeuN expression, but did not influence BDNF and pRaf-1 expression. Conclusion Overall, our study results indicated that EA at acupoints, initiated 1 d postreperfusion, upregulates BDNF expression to provide BDNF-mediated neuroprotection against caspase-3-dependent neuronal apoptosis through activation of the Raf-1/MEK1/2/ERK1/2/p90RSK/Bad signaling cascade after 3 d of reperfusion in mild MCAo.

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