Neural Regeneration Research ›› 2018, Vol. 13 ›› Issue (9): 1594-1601.doi: 10.4103/1673-5374.235294

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Electroacupuncture exerts neuroprotective effects on ischemia/reperfusion injury in JNK knockout mice: the underlying mechanism

Chun-Xiao Wu1, 2, Yi-Hui Feng3, Lu Yang1, 4, Zhu-Lian Zhan4, Xiu-Hong Xu4, Xiao-Ying Hu4, Zhi-Hua Zhu5, Guo-Ping Zhou1, 4   

  1. 1 School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong Province, China
    2 Medical College of Acu-Moxi and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong Province, China
    3 Central Hospital of Qingdao, Qingdao, Shandong Province, China
    4 Traditional Chinese Medicine-Integrated Hospital, the Affiliated Hospital of Southern Medical University, Guangzhou, Guangdong Province,China
    5 Ruikang Hospital Affiliated to Guangxi College of Traditional Chinese Medicine, Nanning, Guangxi Zhuang Autonomous Region, China
  • Received:2018-04-02 Online:2018-09-15 Published:2018-09-15
  • Contact: Guo-Ping Zhou, M.D.,doctorzgp@sina.com
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 81173355.

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Abstract:

Simple regulation of c-Jun N-terminal kinase (JNK) or p38 mitogen-activated protein kinase (MAPK) pathways is not enough to trigger cell apoptosis. However, activation of the stress activated pathway (JNK/p38 MAPK) together with inhibition of the growth factor activated extracellular signal-regulated kinase (ERK) pathway can promote cell apoptosis. We hypothesized that inhibition of the JNK or p38 pro-apoptotic pathway and activating the ERK pathway could be the mechanism of anti-apoptosis following cerebral ischemia/reperfusion injury. To investigate the mechanism of the protective effect of electroacupuncture on cerebral ischemia/reperfusion injury in JNK knockout mice, mouse models of cerebral ischemia/reperfusion injury were established by Longa’s method. Electroacupuncture was conducted at acupoints Chize (LU5), Hegu (LI4), Sanyinjiao (SP6) and Zusanli (ST36) 1.5 hours after ischemia/reperfusion injury for 20 minutes,once a day. The neurological function was evaluated using neurological deficit scores. The expression of phospho-extracellular signal-regulated kinase (p-ERK) and phospho-p38 (p-p38) in JNK knockout mice was detected using double-labeling immunofluorescence and western blot assay. The mRNA expression of ERK and p38 was measured by quantitative real-time polymerase chain reaction. Electroacupuncture improved neurological function, increased the immunoreactivity and relative expression of p-ERK and reduced that of p-p38 in the cerebral cortex and hippocampus on the injured side. Electroacupuncture increased mRNA expression of ERK, but decreased that of p38 in the cerebral cortex and hippocampus on the injured side. In conclusion, electroacupuncture upregulated the protective ERK pathway and inhibited the pro-apoptotic p38 pathway, thereby exerting a neuroprotective effect and improving the neurological function in JNK knockout mice.

Key words: nerve regeneration, MAPKs signaling pathway, cerebral ischemia/reperfusion, stress-activated pathway, growth factor-activated pathway, electroacupuncture, apoptosis