Electroacupuncture Promoting Axonal Regeneration in Spinal Cord Injury Rats via Suppression of Nogo/NgR and Rho/ROCK Signaling Pathway
Received 23 May 2019
Accepted for publication 8 October 2019
Published 13 December 2019 Volume 2019:15 Pages 3429—3442
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Yuping Ning
Wei-Ping Xiao,1,* Li-Li-Qiang Ding,2,* You-Jiang Min,1,3 Hua-Yuan Yang,4 Hai-Hua Yao,3 Jie Sun,1 Xuan Zhou,1 Xue-Bo Zeng,1 Wan Yu1
1Spinal Department of Orthopedics and Department of Acupuncture, Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi, People’s Republic of China; 2Department of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China; 3Department of Traditional Chinese Medicine, Shanghai Eighth People’s Hospital, Shanghai, People’s Republic of China; 4Institute of Traditional Chinese Medicine Engineering, Shanghai University of Traditional Chinese Medicine, Shanghai, People’s Republic of China
*These authors contributed equally to this work
Correspondence: You-Jiang Min
Shanghai Eighth People’s Hospital, Caobao Road 8, Shanghai 200235, People’s Republic of China
Tel +86 18221786381
Shanghai University of Traditional Chinese Medicine, Cairen Road 1200, Shanghai 201203, People’s Republic of China
Tel +86 13651968830
Purpose: To observe the changes of Nogo/NgR and Rho/ROCK signaling pathway-related gene and protein expression in rats with spinal cord injury (SCI) treated with electroacupuncture (EA) and to further investigate the possible mechanism of EA for treating SCI.
Methods: Allen’s method was used to create the SCI rat model. Sixty-four model rats were further subdivided into four subgroups, namely, the SCI model group (SCI), EA treatment group (EA), blocking agent Y27632 treatment group (Y27632) and EA+blocking agent Y27632 treatment group (EA+Y), according to the treatment received. The rats were subjected to EA and/or blocking agent Y27632 treatment. After 14 days, injured spinal cord tissue was extracted for analysis. The mRNA and protein expression levels were determined by real-time fluorescence quantitative PCR and Western blotting, respectively. Cell apoptosis changes in the spinal cord were evaluated by in situ hybridization. Hindlimb motor function in the rats was evaluated by Basso-Beattie-Bresnahan assessment methods.
Results: Except for RhoA protein expression, compared with the SCI model group, EA, blocking agent Y27632 and EA+blocking agent Y27632 treatment groups had significantly reduced mRNA and protein expression of Nogo-A, NgR, LINGO-1, RhoA and ROCK II in spinal cord tissues, increased mRNA and protein expression of MLCP, decreased p-MYPT1 protein expression and p-MYPT1/MYPT1 ratio, and caspase3 expression, and improved lower limb movement function after treatment for 14 days (P<0.01 or <0.05). The combination of EA and the blocking agent Y27632 was superior to EA or blocking agent Y27632
treatment alone (P < 0.01 or <0.05).
Conclusion: EA may have an obvious inhibitory effect on the Nogo/NgR and Rho/ROCK signaling pathway after SCI, thereby reducing the inhibition of axonal growth, which may be a key mechanism of EA treatment for SCI.
Keywords: Nogo/NgR, Rho/ROCK, MLCP, MYPT1, spinal cord injury, Y27632, electroacupuncture
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