PKC[beta]II-induced upregulation of PGP9.5 and VEGF in postoperative persistent pain in rats

• Published in: Journal of pain research 2018-01, Vol.11, p.2095
• Main Authors: Zhu, Xiang, Liu, Yuxi, Huang, Hongfang, Zhang, Yonghua, Huang, Saisai, Zhou, Weiwei, Bian, Xiaocui, Shen, Shiren, Cao, Su
• Format: Article
• Language: English
• Subjects: Endothelial growth factors; Endothelium; Fluorescent antibody technique; Ganglion cysts; Genes; Neurons; Peptides; Postoperative pain; Protein kinases; Surgery; Vascular endothelial growth factor
• ISSN: 1178-7090; 1178-7090
• DOI: 10.2147/JPR.S144852

Purpose: Postoperative pain is a common clinical problem. In this study, we aimed to investigate the role of protein kinase C [beta]II (PKC[beta]II) 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-PKC[beta]II were observed in dorsal root ganglion (DRG) or spinal cord from SMIR-operated rats by Western blotting and immunofluorescence. In addition, the effects of PKC[beta]II 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 PKC[beta]II. Moreover, mechanical withdrawal threshold (MWT) was assessed before or after SMIR-operated rats were treated with inhibitor or activator of PKC[beta]II. Results: The expression of PKC[beta]II in DRG and spinal cord was significantly increased after SMIR surgery (P < 0.001, P < 0.01) and expression of PKC[beta]II 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 PKC[beta]II and a significant decrease of MWT (P < 0.001, P < 0.05). The activator of PKC[beta]II greatly increased the expression of PGP9.5 and VEGF (P < 0.05, P < 0.01) and enhanced MWT (P < 0.001), while inhibitor of PKC[beta]II decreased the expression of PGP9.5 and VEGF and attenuated MWT (P < 0.05, P < 0.01, P < 0.001). Conclusion: Activation of PKC[beta]II signaling pathways might be an important mechanism in the progression of postoperative pain. Keywords: postoperative persistent pain, neurons, PKC[beta]II, PGP9.5, VEGF