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首页> 外文期刊>Pain research & management: the journal of the Canadian Pain Society = journal de la socie?te? canadienne pour le traitement de la douleur >Microglial BDNF, PI3K, and p-ERK in the Spinal Cord Are Suppressed by Pulsed Radiofrequency on Dorsal Root Ganglion to Ease SNI-Induced Neuropathic Pain in Rats
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Microglial BDNF, PI3K, and p-ERK in the Spinal Cord Are Suppressed by Pulsed Radiofrequency on Dorsal Root Ganglion to Ease SNI-Induced Neuropathic Pain in Rats

机译：脊髓背根神经节上的脉冲射频抑制脊髓中的小胶质细胞BDNF，PI3K和p-ERK，从而减轻大鼠SNI引起的神经性疼痛

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Background. Pulsed radiofrequency (PRF) on the dorsal root ganglion (DRG) has been applied to alleviate neuropathic pain effectively, yet the mechanisms underlying pain reduction owing to this treatment are not clarified completely. The activated microglia, brain-derived neurotrophic factor (BDNF), phosphatidylinositol 3-kinase (PI3K), and phosphorylated extracellular signal-regulated kinase (p-ERK) in the spinal cord were demonstrated to be involved in developing neuropathic pain. Also, it has been just known that PRF on DRG inhibits the microglial activation in nerve injury rats. Here, we aim to investigate whether PRF treatment could regulate the levels of BDNF, PI3K, and p-ERK in the spinal cord of rats with spared nerve injury (SNI) via suppressing the spinal microglia activation to ease neuropathic pain. Methods. The rats with SNI were intrathecally treated with minocycline (specific microglia inhibitor) or same volume of dimethyl sulfoxide once daily, beginning from 1?h before nerve transection to 7 days. PRF was applied adjacent to the L4-L5 DRG of rats with SNI at 45?V for 6?min on the seventh postoperative day, whereas the free-PRF rats were treated without PRF. The withdrawal thresholds were studied, and the spinal levels of ionized calcium-binding adapter molecule 1 (Iba1), BDNF, PI3K, and p-ERK were calculated by western blot analysis, reverse transcription-polymerase chain reaction, and immunofluorescence. Results. The paw withdrawal mechanical threshold and paw withdrawal thermal latency decreased in the ipsilateral hind paws after SNI, and the spinal levels of Iba1, BDNF, PI3K, and p-ERK increased on day 21 after SNI compared with baseline (). An intrathecal injection of minocycline led to the reversal of SNI-induced allodynia and increase in levels of Iba1, BDNF, PI3K, and p-ERK. Withdrawal thresholds recovered partially after a single PRF treatment for 14 days, and SNI-induced microglia hyperactivity, BDNF upregulation, and PI3K and ERK phosphorylation in the spinal cord reduced on D14 due to the PRF procedure. Conclusion. Microglial BDNF, PI3K, and p-ERK in the spinal cord are suppressed by the therapy of PRF on DRG to ease SNI-induced neuropathic pain in rats.
机译：背景。背根神经节（DRG）上的脉冲射频（PRF）已被有效地缓解神经性疼痛，但由于这种治疗而导致的疼痛减轻的机制尚未完全阐明。激活的小胶质细胞，脑源性神经营养因子（BDNF），磷脂酰肌醇3-激酶（PI3K）和脊髓中的磷酸化细胞外信号调节激酶（p-ERK）参与了发展性神经性疼痛。同样，已经知道DRG上的PRF抑制神经损伤大鼠中的小胶质细胞活化。在这里，我们旨在研究PRF治疗是否可以通过抑制脊髓小胶质细胞活化以减轻神经性疼痛来调节具有幸存神经损伤（SNI）的大鼠脊髓中BDNF，PI3K和p-ERK的水平。方法。从神经横断前1小时开始至7天，每天一次用米诺环素（特异性小胶质细胞抑制剂）或相同体积的二甲基亚砜在鞘内治疗SNI大鼠。在术后第7天，在SNI为45？V的大鼠的L4-L5 DRG旁施加PRF 6分钟，而游离PRF大鼠则不使用PRF。研究了戒断阈值，并通过蛋白质印迹分析，逆转录-聚合酶链反应和免疫荧光计算了离子化钙结合衔接子分子1（Iba1），BDNF，PI3K和p-ERK的脊髓水平。结果。与基线相比，SNI后同侧后爪的爪退出机械阈值和爪退出热潜伏期降低，并且在SNI后第21天，脊柱中Iba1，BDNF，PI3K和p-ERK的水平升高。鞘内注射米诺环素可逆转SNI诱导的异常性疼痛，并增加Iba1，BDNF，PI3K和p-ERK的水平。单次PRF治疗14天后，戒断阈值部分恢复，由于PRF程序，D14导致SNI诱导的小胶质细胞过度活跃，BDNF上调以及脊髓中PI3K和ERK磷酸化降低。结论。脊髓中的小胶质细胞BDNF，PI3K和p-ERK可通过对DRG进行PRF治疗来缓解，以减轻SNI诱导的大鼠神经性疼痛。

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