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PKCβII-induced upregulation of PGP9.5 and VEGF in postoperative persistent pain in rats

Authors Zhu X, Liu Y, Huang H, Zhang Y, Huang S, Zhou W, Bian X, Shen S, Cao S

Received 26 June 2017

Accepted for publication 3 April 2018

Published 27 September 2018 Volume 2018:11 Pages 2095—2106

DOI https://doi.org/10.2147/JPR.S144852

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Katherine Hanlon


Xiang Zhu,* Yuxi Liu,* Hongfang Huang, Yonghua Zhang, Saisai Huang, Weiwei Zhou, Xiaocui Bian, Shiren Shen, Su Cao

Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, People’s Republic of China

*These authors contributed equally to this work

Purpose: Postoperative pain is a common clinical problem. In this study, we aimed to investigate the role of protein kinase C bII (PKCβII) in the progression of postoperative pain following skin/muscle incision and retraction (SMIR) surgery.
Materials and methods: SMIR postoperative pain model was established in rats, akin to a clinical procedure. The expression level and location of p-PKCβII were observed in dorsal root ganglion (DRG) or spinal cord from SMIR-operated rats by Western blotting and immunofluorescence. In addition, the effects of PKCβII on the expression of protein gene product 9.5 (PGP9.5) or vascular endothelial growth factor (VEGF) were assessed by using pharmacological activator and inhibitor of PKCβII. Moreover, mechanical withdrawal threshold (MWT) was assessed before or after SMIR-operated rats were treated with inhibitor or activator of PKCβII. 
Results: The expression of PKCβII in DRG and spinal cord was significantly increased after SMIR surgery (P < 0.001, P < 0.01) and expression of PKCβII was located in the neurons of the spinal cord, and magnocellular neurons, non-peptide neurons, and peptide neurons in DRG. Besides, compared with skin/muscle incision group, retraction caused a marked increase in the expression of PKCβII and a significant decrease of MWT (P < 0.001, P < 0.05). The activator of PKCβII greatly increased the expression of PGP9.5 and VEGF (P < 0.05, P < 0.01) and enhanced MWT (P < 0.001), while inhibitor of PKCβII decreased the expression of PGP9.5 and VEGF and attenuated MWT (P < 0.05, P < 0.01, P < 0.001).
Conclusion: Activation of PKCβII signaling pathways might be an important mechanism in the progression of postoperative pain.

Keywords: postoperative persistent pain, neurons, PKCβII, PGP9.5, VEGF

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