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物理综合治疗对脑梗死患者血清炎性细胞因子及功能恢复的影响 被引量:3

Effects of Combined Physical Therapy on Serum Inflammatory Cytokines in Patients with Cerebral Infarction and Function Recovery
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摘要 目的:观察物理综合治疗对脑梗死患者血清IL-1β、IL-6、TNF-α和hs-CRP的影响,探讨物理综合治疗脑梗死的可能机制。方法:60例脑梗死患者随机分为综合组和药物组各30例,分别给予超声波、激光、低频电疗及药物等综合治疗与单纯药物治疗,另设健康体检职工30例为正常对照(正常组)。结果:治疗前血清IL-1β、IL-6、TNF-α和hs-CRP含量,综合组及药物组均显著高于正常组(P<0.01);治疗10 d后,2组与治疗前比较均显著降低(P<0.01),但仍高于正常组;2组间比较,综合组下降更明显(P<0.05)。BI及FMA评分与治疗前比较,2组均有提高,2组间比较,综合组更显著(均P<0.05)。结论:脑梗死患者体内存在炎症改变,综合物理治疗可显著提高临床疗效,其机制可能与降低IL-1β、IL-6、TNF-α及hs-CRP含量、促进自由基的清除和内皮功能修复、改善供血等多种因素有关。 Objective:To observe the effects of combined physical therapy on IL-1β, IL-6, TNF-α and hs-CRP in patients with cerebral infarction and investigate the possible mechanisms of combined physical therapy in the treatment of cerebral infarction. Methods:Sixty patients with cerebral infarction were randomly divided into two groups, combined physical therapy group (ultrasound + laser + low frequency electric therapy + drugs, n=30) and single drug group (n=30). Serum IL-1β, IL-6, TNF-α and hs-CRP levels before and after therapies were determined by ELISA. Results: Before therapies, serum IL-1β, IL-6, TNF-α and hs-CRP in patients with cerebral infarction were significantly higher than those in normal controls (P〈0.01). After therapies, serum IL-1β, IL-6, TNF-α and hs-CRP levels in both two groups were decreased (P〈0.01). The IL-1β, IL-6, TNF-α and hs-CRP levels in combined physical therapy group were significantly lower than in single drug group (P〈0.05). Conclusion: Patients with cerebral infarction have inflammation changes. The combined physical therapy can obviously improve the clinical curative effectiveness, which is possibly contributed to the fact that it can reduce the levels of IL-1β, IL-6, TNF-α and bs-CRP, eliminate free radicals, facilitate endothelial recovery, and improve blood supply.
出处 《中国康复》 2009年第2期88-90,共3页 Chinese Journal of Rehabilitation
基金 湛江市科委科技计划项目(湛财工2006-95号)
关键词 物理治疗 脑梗死 IL-1Β IL-6 TNF-α HS-CRP R743.3 physical therapy cerebral infarction IL-1β IL-6 TNF-α hs-CRP
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