江苏省科技期刊可视化阅读平台

导航条

江苏科技信息 ›› 2019, Vol. 36 ›› Issue (1): 52-57.doi: 10.1004-7530/2019-36-1-52

• 应用技术 • 上一篇    下一篇

（E）-2-（4-氯苯基）-1-（2,4-2羟基苯）乙酰基肟改善大鼠急性痛风性关节炎的分子机制研究

王毅兵1,彭霁2,*   

  1. 1. 江苏医药职业学院,江苏 盐城 224005
    2. 盐城协和医院,江苏 盐城 224005
  • 出版日期:2019-01-10 发布日期:2019-07-09
  • 通讯作者: 彭霁
  • 作者简介:王毅兵（1976— ）,男,江苏盐城人,实验师,学士;研究方向：药理学。
  • 基金资助:
    盐城市科技计划项目医药类资助;项目名称：兼具降尿酸活性的免疫抑制剂防治痛风的分子机制研究(项目编号：20143115)

Study on molecular mechanisms by which （E）-2-（4-chlorophenyl）-1-（2,4-dihydroxyphenyl） ethanone oxime improved acute gouty arthritis in rats

Yibing Wang1,Ji Peng2,*   

  1. 1. Jiangsu Vocational College of Medicine, Yancheng 224005, China
    2. Yancheng Xiehe Hospital, Yancheng 224005, China
  • Online:2019-01-10 Published:2019-07-09
  • Contact: Ji Peng

RichHTML

1

PDF

749

摘要：

目的:探讨（E）-2-（4-氯苯基）-1-（2,4-2羟基苯）乙酰基肟（EEO）对急性痛风性关节炎的改善作用及其分子机制。方法:随机将大鼠分为正常组、模型组、EEO各剂量组（低、中、高）、秋水仙碱组,各组分别用相应药物灌胃3 d。第3天给药1 h后向大鼠踝关节腔注入尿酸钠晶体（MSU）,观察大鼠关节肿胀度变化。24 h后取滑膜组织,ELISA检测组织中白细胞介素1β和肿瘤坏死因子α的水平,蛋白质印迹检测组织中NLRP3炎性小体各组分和TLR4信号通路关键分子的蛋白表达。结果:与正常组比较,模型组关节周径及滑膜组织中IL-1β和TNF-α的含量显著升高,滑膜组织NLRP3,ASC,Caspase-1,TLR4,MyD88的表达和p65 NF-κB的磷酸化水平显著上调,上述异常均能够被EEO和秋水仙碱逆转。结论:EEO通过调节NLRP3炎症小体和TLR4信号通路缓解MSU诱导的急性痛风性关节炎。

关键词: （E）-2-（4-氯苯基）-1-（2, 4-2羟基苯）乙酰基肟, 急性痛风性关节炎, NLRP3炎性小体, TLR4信号通路

Abstract:

Objective:To investigate the effect of （E）-2-（4-chlorophenyl）-1-（2,4-dihydroxyphenyl） ethanone oxime （EEO） on acute gouty arthritis and its molecular mechanism.Methods:Rats are randomly divided into 6 groups: normal group, model group, EEO low-dose group, EEO middle-dose group, EEO high-dose group,colchicine group,which are orally administrated with corresponding drug. Monosodium urate crystals （MSU） are injected into ankle joint of rats 1 h after drug administration on the third day, and variations of joint swelling are observed. Synovial tissues are dissected 24 h after injection, and synovial interleukin-1β （IL-1β） levels and tumor necrosis factor alpha （TNF-α） are detected using ELISA kits, protein expressions of NLRP3 in flammasome components and key factors involved in TLR4 signaling pathways are measured by Western blot.Results:Compared with normal rats, the joint diameters, synovial IL-1β and TNF-α levels are significantly elevated in MSU-induced acute gouty arthritis rats. More importantly, synovial protein expressions of NLRP3, ASC, Caspase-1, TLR4 and MyD88, as well as phosphorylation of p65 NF-κB are obviously up-regulated in model group, which could be reversed by EEO and colchicine treatment.Conclusion:EEO attenuated MSU-induced acute gouty arthritis through regulating expressions of NLRP3 inflammasome and TLR4 signaling pathways.

Key words: （E）-2-（4-chlorophenyl）-1-（2, 4-dihydroxyphenyl）, acute gouty arthritis, NLRP3 inflammasome, TLR4 signaling pathways

中图分类号: