Background. Protein kinase C (PKC), nuclear factor-kappa B p65 (NF-κB p65), and P2X₃ receptor (P2X₃R) play significant roles in the sensitization and transduction of nociceptive signals, which are considered as potential targets for the treatment of neuropathic pain. However, the mechanisms and relationships among them have not been clearly clarified. Methods. 80 rats were randomized and divided into 10 groups (n = 8). Sciatic chronic constriction injury (CCI) rats were intrathecally administered with bisindolylmaleimide I (GF109203X), a PKC-selective antagonist once a day, or pyrrolidine dithiocarbamate (PDTC), an NF-κB inhibitor twice a day. Sham-operated rats were intrathecally administered with saline. Thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT) were evaluated in all the groups before CCI operation (baseline) and on the 1st, 3rd, 7th, 10th, and 14th day after CCI operation. Protein levels of p-PKCα, p-NF-κB p65, and P2X₃R were analyzed in the CCI ipsilateral L_4–6 dorsal root ganglions (DRGs). Results. Intrathecal injection of GF109203X or PDTC alleviated the TWL and MWT in the following 2 weeks after CCI surgery. The protein levels of p-PKCα, p-NF-κB p65, and P2X₃R in the ipsilateral DRGs significantly increased after CCI operation, which could be partly reversed by intrathecal administration of GF109203X or PDTC. Conclusion. The upregulation of p-PKCα, p-NF-κB p65, and P2X₃R expression in the DRGs of CCI rats was involved in the occurrence and development of neuropathic pain. Phosphorylated PKCα and phosphorylated NF-κB p65 regulated with each other. Phosphorylated NF-κB p65 and PKCα have a mutual regulation relationship with P2X₃R, respectively, while the specific regulatory mechanism needs further research.

中文翻译：

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PKC /NF-κB对坐骨神经损伤大鼠背根神经节P2X3受体的调节作用

背景。蛋白激酶C（PKC），核因子-κBp65（NF- κBp65）和P2X ₃受体（P2X ₃ R）在伤害性信号的敏化和转导中起重要作用，被认为是伤害性信号的潜在靶标。神经性疼痛的治疗。但是，它们之间的机制和关系尚未明确阐明。方法。将80只大鼠随机分为10组（n  = 8）。慢性缩窄性损伤（CCI）大鼠鞘内与bisindolylmaleimide I（GF109203X），一个PKC选择性拮抗剂，每天一次，或二硫代氨基甲酸吡咯烷（PDTC），一个NF-施用κB抑制剂一天两次。假手术的大鼠鞘内注射生理盐水。在CCI手术前（基线）以及CCI手术后第1、3、7、10和14天评估所有组的热撤退潜伏期（TWL）和机械撤退阈值（MWT）。对PKC的蛋白水平α，对NF- κ乙P65，和P2X ₃中的R CCI同侧L的分析_4-6背根神经节（的DRG）。结果。鞘内注射GF109203X或PDTC可在CCI手术后的两周内缓解TWL和MWT。对PKC的蛋白水平α，对NF- κ乙P65，和P2X ₃CCI手术后，同侧DRG中的R显着增加，鞘内注射GF109203X或PDTC可部分逆转。结论。对PKC的上调α，对NF- κ乙P65，和P2X ₃ R的表达在CCI大鼠的DRG参与了发生和神经性疼痛的发展。磷酸化PKC α的和磷酸化NF- κ乙p65的相互调节。磷酸化NF- κ乙p65和PKC α具有P2X相互调节关系₃ R，分别，而特异性调节机制还有待于进一步研究。