关键词: Microglia Neuroinflammation Neuropathic pain PFC rTMS

Mesh : Animals Neuralgia / therapy metabolism Prefrontal Cortex / metabolism Male Transcranial Magnetic Stimulation / methods Rats, Sprague-Dawley Microglia / metabolism Neuroinflammatory Diseases / therapy metabolism Sciatic Nerve / injuries Pain Threshold / physiology Rats Disease Models, Animal Cytokines / metabolism

来  源:   DOI:10.1016/j.neuroscience.2024.07.004

Abstract:
The study aimed to assess the analgesic effect of 10 Hz repetitive transcranial magnetic stimulation (rTMS) targeted to the prefrontal cortex (PFC) region on neuropathic pain (NPP) in rats with chronic constriction injury (CCI) of the sciatic nerve, and to investigate the possible underlying mechanism. Rats were randomly divided into three groups: sham operation, CCI, and rTMS. In the latter group, rTMS was applied to the left PFC. Von Frey fibres were used to measure the paw withdrawal mechanical threshold (PWMT). At the end of the treatment, immunofluorescence and western blotting were applied to detect the expression of M1 and M2 polarisation markers in microglia in the left PFC and sciatic nerve. ELISA was further used to detect the concentrations of inflammation-related cytokines. The results showed that CCI caused NPP in rats, reduced the pain threshold, promoted microglial polarisation to the M1 phenotype, and increased the secretion of pro-inflammatory and anti-inflammatory factors. Moreover, 10 Hz rTMS to the PFC was shown to improve NPP induced by CCI, induce microglial polarisation to M2, reduce the secretion of pro-inflammatory factors, and further increase the secretion of anti-inflammatory factors. Our data suggest that 10 Hz rTMS can alleviate CCI-induced neuropathic pain, while the underlying mechanism may potentially be related to the regulation of microglial M1-to-M2-type polarisation to regulate neuroinflammation.
摘要:
该研究旨在评估10Hz重复经颅磁刺激(rTMS)靶向前额叶皮质(PFC)区域对坐骨神经慢性缩窄性损伤(CCI)大鼠神经性疼痛(NPP)的镇痛作用。并研究可能的潜在机制。大鼠随机分为三组:假手术,CCI和rTMS。在后一组中,将rTMS应用于左PFC。VonFrey纤维用于测量爪缩回机械阈值(PWMT)。在治疗结束时,免疫荧光和免疫印迹法检测左侧PFC和坐骨神经小胶质细胞中M1和M2极化标记物的表达。进一步使用ELISA检测炎症相关细胞因子的浓度。结果显示CCI引起大鼠NPP,降低疼痛阈值,促进小胶质细胞极化至M1表型,并增加促炎和抗炎因子的分泌。此外,10HzrTMS至PFC显示改善CCI诱导的NPP,诱导小胶质细胞极化至M2,减少促炎因子的分泌,并进一步增加抗炎因子的分泌。我们的数据表明,10HzrTMS可以缓解CCI引起的神经性疼痛,而潜在的机制可能与调节小胶质细胞M1至M2型极化以调节神经炎症有关。
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