畜牧与饲料科学 ›› 2014, Vol. 35 ›› Issue (5): 1-1.doi: 10.12160/j.issn.1672-5190.2014.05.002

• 基础科学 • 上一篇    下一篇

连翘酯苷A抗大鼠类风湿性关节炎机制研究

程广东[1] 吕冬云[1] 刘立新[2] 王波[1] 王伟娥[2] 张伟[2] 刘德江[1] 朱德全[1] 岳丽红[1]   

  1. [1]佳木斯大学生命科学学院,黑龙江佳木斯154007 [2]佳木斯大学药学院,黑龙江佳木斯154007
  • 出版日期:2014-05-20 发布日期:2014-05-20
  • 通讯作者: 程广东
  • 作者简介:程广东(1978-),男,讲师,博士研究生,主要研究方向为中药抗炎机制。 通讯作者:岳丽红(1964-),女,副教授,硕士生导师,主要从事微生物学与免疫学的教学与科研工作。
  • 基金资助:
    黑龙江省卫生厅科研课题项目(2012-267);佳木斯大学青年基金项目(Sq2013-028):国家自然科学基金青年项目(31101250).

Study on the Inhibitory Mechanism of Forsythiaside A against Rheumatoid Arthritis of Rats

CHENG Guang-dong,LU Dong-yun,LIU Li-xin,WANG Bo,WANG Wei-e,ZHANG Wei,LIU De- jiang, ZHU De-quan, YUE Li-hong (1.College of Life Science, Jiamusi University,Jiamusi 154007,China;2.College of Pharmacy,Jiamusi University,Jiamusi 154007, China)   

  • Online:2014-05-20 Published:2014-05-20

摘要: [目的]探讨连翘酯苷A对类风湿性关节炎大鼠的抗炎作用及作用原理。[方法]将30只SD大鼠[体重(120±2)g],随机分成3组,每组10只,分别为对照组(A组)、类风湿性关节炎组(B组)和连翘酯苷A治疗组(C组)。首先构建大鼠类风湿性关节炎模型,再观察各组大鼠临床症状、血清中TNF-α蛋白表达量、抗氧化酶和自由基含量。[结果]类风湿性关节炎模型组大鼠血清中TNF-α蛋白表达量增加,SOD含量下降,NO含量上升:而连翘酯苷A治疗组上述指标的趋势正好与之相反。[结论]连翘酯苷A可通过抑制炎症因子TNF—α的含量。并干扰TNF—α蛋白的翻译,影响抗氧化酶及自由基含量,最终发挥抗炎功效。

Abstract: [ Objective ]The research aimed to study the inhibition and inhibitory mechanism of forsythiaside A against rheumatiod arthritis of rat. [ Method ] Thirty SD rats with the weight of (120±2) g were randomly divided into three groups with 10 rats in each group: control group (A group), rheumatiod arthritis group (B group) and forsythiaside A therapy group (C group). The rheumatoid arthritis rat model was constructed to observe the clinical symptoms of rats, the expression amount of TNF-α protein in the serum, antioxidase and free radicals contents in each group. [Result] The expression amount of TNF-α protein in the serum of rats increased in rheumatoid arthritis model group, SOD content decreased and NO content increased. The trends of the above indices were on the contrary in forsythiaside A therapy group. [Conclusion ] Forsythiaside A could affect the contents of TNF-α protein and free radicals by inhibiting the content of TNF-α of inflammatory factor, and interferential the translation of TNF-α protein, eventually the anti-inflammatory effect was obtained.

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