电针调控脊髓损伤后大鼠巨噬细胞表型对炎症反应的影响

发布时间：2019-07-05 19:58

【摘要】：背景:脊髓损伤是一类严重的创伤性疾病,有较高的致残率和死亡率,脊髓损伤目前在临床上仍没有确切有效的治疗方法。因此脊髓损伤是基础医学和临床医学研究热点。脊髓损伤分为原发性损伤和继发性损伤,继发性损伤病理生理机制较为复杂且带来脊髓损害严重。巨噬细胞和小胶质细胞是脊髓损伤部位重要的效应细胞。M1型巨噬细胞可以增强体内的固有免疫反应以清除损伤部位的外部微生物和受损的组织碎片;M2型巨噬细胞具有组织修复和减少炎症因子产生的特性。脊髓损伤后,督脉电针通过调节损伤部位M1/M2巨噬细胞的比例,抑制损伤部位的炎症反应,而神经营养因子-3(NT-3)很可能参与这一过程。对督脉穴位电针刺激可以作为脊髓损伤后的一种辅助治疗。目的:观察电针调控脊髓损伤后大鼠的巨噬细胞表型对炎症反应的影响并对其机制进行初步探讨。方法:16只SD大鼠在T10脊髓节段进行离断以制作脊髓损伤动物模型。另外8只大鼠作为对照组。10只存活大鼠被分为两组,每组各5只。脊髓损伤(SCI)组大鼠在脊髓离断后不接受任何处理;脊髓损伤加电针(SCI+EA)组大鼠在其督脉GV6、GV9处接受电针刺激。我们采用BBB评分评价电针对大鼠功能改善影响的作用,并检测肿瘤坏死因子-α(tumour necrosis factor-α,TNF-α),白细胞介素-1β(interleukin-1β,IL-1β),白细胞介素-6(interleukin-6,IL-6)和白细胞介素-10(interleukin-10,IL-10)的表达等,计数M1/M2巨噬细胞的比例,并进一步探讨其可能的机制。结果:电针提高了脊髓损伤大鼠的BBB评分,下调了M1标记物CD86的表达,降低了M1巨噬细胞的比例,且下调了TNF-α、IL-1β、IL-6的水平。相反,电针上调了M2标记物CD206得表达,提高了M2的比例,上调了抗炎因子IL-10的水平,并且促进了神经营养因子-3(NT-3)的表达。结论:电针刺激对脊髓损伤大鼠的功能恢复具有积极的作用,这可能与损伤局部上调的NT-3发挥神经保护作用有关,而NT-3可能通过上调M2巨噬细胞的比例发挥作用。
[Abstract]:Background: spinal cord injury is a serious traumatic disease with high disability rate and mortality. There is still no accurate and effective treatment for spinal cord injury. Therefore, spinal cord injury is a hot spot in basic medicine and clinical medicine. Spinal cord injury is divided into primary injury and secondary injury. The pathophysiological mechanism of secondary injury is complex and the spinal cord injury is serious. Macrophages and microglia are important effector cells in spinal cord injury. M1 macrophages can enhance the innate immune response in vivo to remove external microorganisms and damaged tissue fragments at the injured site. M2 macrophages have the characteristics of tissue repair and reducing the production of inflammatory factors. After spinal cord injury, du Mai EA can inhibit the inflammatory response by regulating the proportion of M1/M2 macrophages in the injured site, and neurotrophic factor-3 (NT-3) is likely to be involved in this process. Acupuncture stimulation at Dumai acupoint can be used as an auxiliary treatment after spinal cord injury. Aim: to observe the effect of EA on inflammatory response in rats with spinal cord injury (sci) and to explore its mechanism. Methods: sixteen SD rats were severed in T 10 spinal cord segment to establish the animal model of spinal cord injury. The other 8 rats served as the control group. Ten surviving rats were divided into two groups with 5 rats in each group. Spinal cord injury rats in (SCI) group did not receive any treatment after spinal cord transection, and rats in spinal cord injury plus electro-acupuncture (SCI EA) group were stimulated by electro-acupuncture at GV6,GV9 of spinal cord injury. We used BBB score to evaluate the effect of acupuncture on functional improvement in rats, and detected the expression of tumor necrosis factor-伪 (tumour necrosis factor- 伪 (TNF- 伪), interleukin-1 尾 (IL-1 尾), IL-6 (interleukin-6,IL-6) and IL-10 (interleukin-10,IL-10). The proportion of M1/M2 macrophages was counted and the possible mechanism was further discussed. Results: EA increased the BBB score of spinal cord injury rats, down-regulated the expression of M1 marker CD86, decreased the proportion of M1 macrophages, and down-regulated the levels of TNF- 伪, IL-1 尾 and IL-6. On the contrary, EA up-regulated the expression of M2 marker CD206, increased the proportion of M2, upregulated the level of anti-inflammatory factor IL-10, and promoted the expression of neurotrophic factor-3 (NT-3). Conclusion: EA stimulation has a positive effect on the functional recovery of spinal cord injury rats, which may be related to the neuroprotective effect of locally upregulated NT-3, while NT-3 may play a role by up-regulating the proportion of M2 macrophages.
【学位授予单位】：安徽医科大学
【学位级别】：博士
【学位授予年份】：2017
【分类号】：R651.2

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