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脉冲射频调节伤害性通路中疼痛调节基因的表达。

Pulsed radiofrequency modulates pain regulatory gene expression along the nociceptive pathway.

机构信息

Millennium Pain Center, Bloomington, IL; and Biology Department, Illinois State University, Normal, IL; Psychology Department, Illinois Wesleyan University, Bloomington, IL; Teknon Medical Center, Barcelona, Spain; and Anesthesiology Department, Medical S.

出版信息

Pain Physician. 2013 Sep-Oct;16(5):E601-13.

Abstract

BACKGROUND

Pulsed radiofrequency (PRF) therapy is a clinical treatment utilizing electromagnetic energy aimed to relieve neuropathic pain. This is the first study examining the modulated expression of pain regulatory genes following the induction of the spared nerve injury (SNI) pain model and subsequently treated with PRF therapy.

OBJECTIVES

The present study investigated the behavioral efficacy of PRF therapy in rats exhibiting sciatic nerve injury and examined gene expression changes in the sciatic nerve, ipsilateral L5 dorsal root ganglia (DRG), and spinal cord.

STUDY DESIGN

A randomized, experimental trial.

SETTING

Department of Biological Sciences, Illinois State University and Department of Psychology, Illinois Wesleyan University.

METHODS

An SNI model was used in male Sprague-Dawley rats (weight 260-310 g). A sham surgery was also performed as a control group. After 3 days development of the SNI model, an RF electrode was applied to the sciatic nerve proximal to the site of injury and stimulated for 3 minutes. The response to mechanical stimuli was assessed throughout the duration of the study. Furthermore, changes in gene expression along the nociceptive tract (sciatic nerve, DRG, and spinal cord) were assessed 24 hours post-PRF therapy.

RESULTS

It was observed that the mechanical allodynia, induced by SNI model, was reversed to control values within 24 hours post-PRF therapy. Additionally, modulated expression of pain regulatory genes was observed after induction of the SNI model. Following PRF therapy, expression of many of these genes returned to control values (sham) in each of the tissues tested. Increased proinflammatory gene expression, such as TNF-α and IL-6, observed in the sciatic nerve (site of injury) in the SNI group was returned to baseline values following PRF therapy. Up-regulation of GABAB-R1, Na/K ATPase, and 5-HT3r as well as down regulation of TNF-α and IL-6 were also observed in the DRG in the SNI-PRF group relative to the SNI group. Up-regulation of Na/K ATPase and c-Fos was found in the spinal cord following PRF treatment relative to the SNI group.

LIMITATIONS

Immediate changes in gene expression were observed at 24 hours to better determine the mechanism with no long-term data at this time. Protein expression was not assessed in addition to gene expression changes.

CONCLUSION

These results indicate that the electromagnetic energy applied via PRF therapy influences the reversal of behavioral and molecular effects of hypersensitivity developed from a peripheral nerve injury.

摘要

背景

脉冲射频(PRF)治疗是一种利用电磁能缓解神经病理性疼痛的临床治疗方法。这是第一项研究,旨在观察在 spared nerve injury(SNI)疼痛模型诱导后,经 PRF 治疗后疼痛调节基因的调制表达。

目的

本研究旨在探讨 PRF 治疗对坐骨神经损伤大鼠的行为疗效,并检测坐骨神经、同侧 L5 背根神经节(DRG)和脊髓中基因表达的变化。

研究设计

随机、实验性试验。

地点

伊利诺伊州立大学的生物科学系和伊利诺伊卫斯理大学的心理学系。

方法

采用雄性 Sprague-Dawley 大鼠(体重 260-310g)建立 SNI 模型。同时也进行了假手术作为对照组。在 SNI 模型建立 3 天后,将射频电极应用于损伤部位近端的坐骨神经并刺激 3 分钟。在整个研究过程中评估对机械刺激的反应。此外,在 PRF 治疗后 24 小时评估沿伤害性通路(坐骨神经、DRG 和脊髓)的基因表达变化。

结果

观察到,SNI 模型诱导的机械性痛觉过敏在 PRF 治疗后 24 小时内恢复到对照值。此外,在 SNI 模型诱导后观察到疼痛调节基因的调制表达。在 PRF 治疗后,在测试的每个组织中,许多这些基因的表达都恢复到对照值(假手术)。在 SNI 组中,在损伤部位的坐骨神经中观察到的促炎基因表达增加,如 TNF-α 和 IL-6,在 PRF 治疗后恢复到基线值。在 SNI-PRF 组中,与 SNI 组相比,在 DRG 中观察到 GABAB-R1、Na/K ATPase 和 5-HT3r 的上调以及 TNF-α 和 IL-6 的下调。在 PRF 治疗后,与 SNI 组相比,在脊髓中观察到 Na/K ATPase 和 c-Fos 的上调。

局限性

为了更好地确定机制,在没有长期数据的情况下,仅在 24 小时内观察到基因表达的即时变化。除了基因表达变化外,未评估蛋白质表达。

结论

这些结果表明,通过 PRF 治疗施加的电磁能影响了外周神经损伤引起的超敏反应的行为和分子效应的逆转。

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