电针对肠易激综合征大鼠结肠和背根神经节卫星神经胶质细胞活性的调节作用

Zhang Fang, Yan Cuina, Weng Zhijun, W U Luyi, Q I Li, Zhao Min, Xin Yuhu, W U Huangan, Liu Huirong
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引用次数: 0

摘要

目的研究卫星神经胶质细胞在肠易激综合征(IBS)中的作用以及电针天枢(ST25)和上巨虚(ST37)的效果:方法:通过刺激结肠直肠胀气(CRD)诱导 IBS 内脏超敏模型。将清洁级雄性 Sprague-Dawley (SD) 大鼠随机分为四组:正常组 (NG)、模型组 (MG)、电针组 (EA) 和神经胶质细胞抑制剂组 (FCA)。第 6 周在天枢(ST25)和上巨虚(ST37)进行双侧 EA(2/100 Hz,1 mA,30 分钟)治疗。腹部退缩反射(AWR)评分用于评估与内脏痛觉减退相关的行为反应,苏木精-伊红染色用于评估结肠的病理变化。使用免疫荧光、免疫组织化学、Western印迹和实时聚合酶链反应分析了结肠和结肠相关背根神经节(DRG)中神经胶质纤维酸性蛋白(GFAP)的蛋白和mRNA水平。通过全细胞膜片钳分析观察了EA对结肠相关DRG神经元电生理特性的影响:结果:EA能明显降低肠易激综合征大鼠在分级(20、40、60、80 mm Hg)CRD刺激下的内脏疼痛行为评分。此外,EA 还下调了肠易激综合征大鼠结肠和结肠相关 DRG 中 GFAP 蛋白和 mRNA 的表达水平。EA还能调节肠易激综合征大鼠结肠相关DRG神经元的静息膜电位、流变基和动作电位:结论:EA能通过下调结肠和结肠相关DRG中GFAP蛋白和mRNA的表达来调节结肠相关DRG神经元的兴奋性,这表明EA能缓解肠易激综合征大鼠内脏超敏反应的潜在神经生物学机制。
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Regulatory role of electroacupuncture on satellite glial cell activity in the colon and dorsal root ganglion of rats with irritable bowel syndrome.

Objective: To investigate the role of satellite glial cells in irritable bowel syndrome (IBS) and the effect of electroacupuncture (EA) at the Tianshu (ST25) and Shangjuxu (ST37) combination.

Methods: A model for visceral hypersensitivity in IBS was induced through colorectal distension (CRD) stimulation. Clean-grade male Sprague-Dawley (SD) rats were randomly divided into four groups: a normal group (NG), a model group (MG), an electroacupuncture group (EA), and a glial cell inhibitor group (FCA). Bilateral EA (2/100 Hz, 1 mA, 30 min) was administered at the Tianshu (ST25) and Shangjuxu (ST37) in week 6. Abdominal withdrawal reflex (AWR) scores were used to assess the behavioral response associated with visceral hyperalgesia, while hematoxylin-eosin staining was employed to evaluate pathological changes in the colon. The protein and mRNA levels of glial fibrillary acidic protein (GFAP) in the colon and colon-related dorsal root ganglion (DRG) were analyzed using immun-ofluorescence, immun-ohistochemistry, Western blotting, real-time polymerase chain reaction. The impact of EA on electrophysiological properties of colon-related DRG neurons was observed through whole-cell patch clamp analysis.

Results: EA significantly reduced the visceral pain behavior scores in rats with IBS in response to graded (20, 40, 60, 80 mm Hg) CRD stimulation. Additionally, EA downregulated the protein and mRNA expression levels of GFAP in the colon and colon-related DRG of rats with IBS. EA also regulated the resting membrane potential, rheobase and action potential of colon-related DRG neurons in rats with IBS.

Conclusions: EA can regulate the excitatory properties of colon-related DRG neurons by downregulating the protein and mRNA expression of GFAP in the colon and colon-related DRG, indicating a potential neurobiological mechanism by which EA relieves visceral hypersensitivity in rats with IBS.

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