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作 者:刘洪柏[1] 张鸣生[1] 区丽明[1] 朱洪翔[1]
机构地区:[1]广东省人民医院(广东省医学科学院)康复科,广州510080
出 处:《中国康复医学杂志》2014年第3期208-211,217,共5页Chinese Journal of Rehabilitation Medicine
摘 要:目的:观察体外冲击波(ESW)对大鼠膝骨关节炎(OA)中白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)的影响,探讨ESW治疗膝骨关节炎的可能机制。方法:将30只SD大鼠随机分为治疗组、模型组、对照组,每组各10只。治疗组和模型组采用单侧后肢跟腱切除法建立膝OA模型,对照组不做任何处理。治疗组造模后立即给予ESW治疗1次,能流密度0.1mJ/mm2,冲击次数1000次。各组大鼠分别于治疗后4周处死,取膝OA关节液和关节软骨,分别采用酶联免疫吸附试验(ELISA)和免疫组化技术法,检测各组膝关节中IL-1β和TNF-α的水平,并比较各组之间的差异。结果:采用ELISA法行关节液IL-1β和TNF-α含量测定,治疗组和模型组较对照组明显增高(P<0.01),治疗结束后治疗组较模型组下降(P<0.05)。免疫组化法关节软骨IL-1β和TNF-α测定,治疗组和模型组阳性率较对照组明显增高(P<0.01),治疗结束后治疗组的阳性率较模型组下降(P<0.05)。结论:膝骨关节炎中IL-1β和TNF-α水平上升,而ESW能下调膝OA大鼠IL-1β、TNF-α的表达,提示可通过降低关节软骨的炎症因子水平,对膝骨关节炎起防治作用。Objective: To observe the effect of extracorporeal shock wave therapy (ESWT) on the expressions of interleu- kin-l[3 (IL-1β) and tumor necrosis factor-α (TNF-α) in cartilage of rats with experimental knee osteoarthritis (OA), and to explore its potential mechanism. Method: Thirty rats were randomly and averagely divided into treatment group, model group and control group. The method of heel tendon resection on unilateral hind limb was used to establish OA animal model. The treatment group was treated with ESWT(each 1000 impulse, energy flux density 0.1mJ/mm2), the control group hadn't any treatment. The rats were sacrificed respectively at 4 weeks after ESWT. The articular genu rinse solution were collected from rats for detecting the expressions of IL-1β and TNF-α in synovia by ELI- SA, and immunohistochemical staining was used to observe the expression characteristics of IL-1β and TNF-α in cartilage of each group, and the differences were compared among the groups. Result: Expressions of both IL-1β and TNF-α were down-regulated significantly in treatment group compared with model group, the difference between the two groups was significant (P〈 0.05). ELISA assay showed the concentrations of IL-1β and TNF-α in joint irrigation of treatment group and model group rose higher than that of control group (P〈 0.01), after ESWT those reduced more in treatment group than in modal group(P〈 0.05), immunohistochemical assay showed the positive rates of IL-β and TNF-α in cartilage rose higher in treat- ment group and model group than that in control group(P〈0.01), after ESWT positive rate reduced more in treatment group than in model group(P 〈 0.05). Conclusion: In KOA the level of IL-1β and TNF-α rose, while ESW could down-regulate the expressions of IL-1β and TNF-α of KOA rats. It suggested by reducing the level of inflammation factors of cartilage ESW might prevent and treat KOA.
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