文章摘要
李高玺,林志健,张 冰,王海鸽,边 猛.高血尿酸状态大鼠痛风性关节炎模型研究[J].,2019,19(11):2007-2012
高血尿酸状态大鼠痛风性关节炎模型研究
Model of Gouty Arthritis in Rats with High Blood Uric Acid Status
投稿时间:2018-11-28  修订日期:2018-12-23
DOI:10.13241/j.cnki.pmb.2019.11.002
中文关键词: 高血尿酸状态  痛风性关节炎  尿酸盐沉积  氧化应激
英文关键词: Hyperuricemia  Gouty arthritis  Uric acid salt dep  Oxidative stress
基金项目:国家重大新药创制专项(2017ZX09301024);国家自然科学基金项目(81673618);北京中医药大学在读研究生资助项目(2018-JYB-XS045)
作者单位E-mail
李高玺 北京中医药大学中药学院 北京100029 ligaoxi33@163.com 
林志健 北京中医药大学中药学院 北京100029  
张 冰 北京中医药大学中药学院 北京100029  
王海鸽 北京中医药大学中药学院 北京100029  
边 猛 北京中医药大学中药学院 北京100029  
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中文摘要:
      摘要 目的:以高尿酸血症为基础,探讨一种接近临床痛风性关节炎发生的模型塑造方法。方法:选择雄性SD大鼠20只,随机分为正常组、模型组。塑造高血尿酸状态大鼠,诱导痛风性关节炎模型。检测两组大鼠踝关节不同时间段肿胀度、炎症分级;检测两组大鼠血清中尿酸及其生成排泄相关指标、血清中氧化应激反应和炎症表达相关指标;观察大鼠踝关节滑膜病理情况。结果:与正常组相比,痛风模型造模48小时内,模型组大鼠踝关节肿胀度显著升高(P<0.05或P<0.01),模型组炎症分级评分较高;实验第21、28 d,模型组大鼠血清UA含量升高(P<0.01);实验第28d,模型组大鼠血清及肝脏中XOD、ADA活性均升高,血清及肝脏MDA表达增多、SOD表达减少(P<0.05或P<0.01);模型组大鼠血清及踝关节组织中IL-1β含量增加;HE染色表明模型组大鼠踝关节有明显病理损伤。结论:在大鼠高血尿酸状态下可诱导急性痛风性关节炎模型,此模型一定程度上符合人类痛风发作过程,并可维持一定的时间。
英文摘要:
      ABSTRACT Objective: Based on hyperuricemia, to explore a method of modeling gouty arthritis in close proximity to clinical gouty arthritis. Methods: 20 male SD rats were randomly divided into 2 groups. Establish hyperuricemia rats. Induce gouty arthritis model. The swelling degree of ankle joints of two groups was detected at different time periods, Inflammatory classification. The serum uric acid and its related indexes in two groups were tested. Indicators related to oxidative stress and inflammatory expression. Synovium pathology of ankle joint in rats were also observed. Results: During the 48 h modeling period, Compared with the normal group, the swelling degree of the ankle joint in the model group increased significantly(P<0.05 or P<0.01). and Inflammation score is higher. The serum UA level in- creasedin the rats of model group on day 21, 28(P<0.01). The activity of XOD and ADA in serum and liver of model group increased significantly in day28 (P<0.05 or P<0.01). Meanwhile, The expression of MDA in serum and liver increased, SOD decreased while the expression of IL-1β in serum and synovial tissue of ankle joint a increased in model group(P<0.05 or P<0.01). HE staining showed that Rats in the model group had obvious pathological injuries. Conclusion: The acute gout model can be successfully induced in the state of high blood uric acid rats. This model is partly consistent with the human gout process and can be maintained for a certain period of time.
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