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作 者:刘宏波[1] 宋振全[2] 梁国标[2] 王志军[2] 赵明光[2] 赵旭[3] 雷伟[2] 李宾[2]
机构地区:[1]阜新市中心医院神经外科,辽宁123000 [2]沈阳军区总医院,辽宁110000 [3]泰山医学院附属医院神经外科,山东泰安271000
出 处:《创伤外科杂志》2015年第2期154-159,共6页Journal of Traumatic Surgery
摘 要:目的研究中分子量羟乙基淀粉(HES 130/0.4,万汶)对脊髓压迫伤后神经源性疼痛的作用。方法 SD雄性成年大鼠48只,随机分为4组,第1组去除T7-8椎板后缝合作对照组,其余3组为大鼠脊髓慢性压迫模型,并经尾静脉分别给予生理盐水、HES 40、HES 130/0.4处理;4组均行行为学检测后肢机械痛敏压力阈值(paw withdraw pressure threshold,PWPT)和热痛敏潜伏期(paw withdraw latency,PWL)变化;静脉注射伊文氏蓝(evens blue,EB)测脊髓组织内EB含量,观察血脊髓屏障(blood spinal cord barrier,BSCB)情况;免疫荧光和免疫印迹法(western blotting)观察星形胶质细胞和巨噬细胞/小胶质细胞活化情况,利用酶联免疫吸附法(ELISA)测定白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)表达水平。结果 HES 130/0.4可以缓解异常通透的BSCB,抑制损伤区域的炎症反应,并下调IL-1、IL-6、TNF-α表达;脊髓损伤后,PWPT和PWL明显降低,给予HES 130/0.4处理后有显著改善。结论 HES 130/0.4对脊髓损伤后并发的神经源性痛有缓解作用,其机制可能为通过改善异常通透的BSCB来抑制其损伤区域的炎症反应。Objective To study the effect of molecular weight of hydroxyethyl starch( HES 130 /0. 4,Wan Men) on neurogenic pain after spinal cord compression injury. Methods Forty-eight adult male SD rats were randomly divided into four groups. The first group was sutured as the control group after removal of T7- 8vertebral plate. The rest three groups of rats were given saline,HES 40,HES 130 /0. 4 treatment as model of chronic spinal cord compression. Four groups were tested for paw withdraw pressure threshold( PWPT) and paw withdraw latency( PWL). Evens Blue( EB) was intravenously injected and the EB content of spinal cord tissue was measured to observe the blood spinal cord barrier( BSCB). Immunofluorescence and western blotting were adopted to observe the activation of astrocytes and microglia / macrophages. ELISA method was conducted to determine the expression of IL-1,IL-6 and TNF-α. Results HES 130 /0. 4 can alleviate abnormally permeable BSCB,inhibit the inflammatory response in the injury site and down-regulate the expression of IL-1,IL-6 and TNF-α. After spinal cord injury,PWPT and PWL decreased significantly. After HES 130 /0. 4 treatment,PWPT and PWL improved significantly. Conclusion HES 130 /0. 4 can relieve neurogenic pain complicated with spinal cord injury. Its mechanism may be through improving the abnormally permeable BSCB to suppress the inflammatory response in the injury site.
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