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

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

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 Pu...

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Bibliographic Details
Main Authors: Zhu X, Liu Y, Huang H, Zhang Y, Huang S, Zhou W, Bian X, Shen S, Cao S
Format: Article
Language:English
Published: Dove Medical Press 2018-09-01
Series:Journal of Pain Research
Subjects:
postoperative persistent pain
neurons
PKCβII
PGP9.5
VEGF
Online Access:https://www.dovepress.com/pkcbetaii-induced-upregulation-of-pgp95-and-vegf-in-postoperative-pers-peer-reviewed-article-JPR
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Summary: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
ISSN:1178-7090

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