| 引用本文:张娜1，赵俊云1，薛慧清2，刘慧1，李彩彩1，杨向竹1，周然2.黄芪糖蛋白对胶原诱导性关节炎小鼠脾组织T-bet及GATA-3表达的影响[J].世界中医药,2017,(05):. |
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| 黄芪糖蛋白对胶原诱导性关节炎小鼠脾组织T-bet及GATA-3表达的影响 |
| Effect of Astragalus Glycoproteins on T-bet and GATA-3 Expression in Mice Spleen with Collagen-induced Arthritis |
| 投稿时间：2016-07-07 |
| DOI：10.3969/j.issn.1673-7202.2017.05.039 |
| 中文关键词: 黄芪糖蛋白 牛Ⅱ型胶原诱导性关节炎小鼠 GATA-3 T-bet |
| English Keywords:Astragalus glycoprotein CIA GATA-3 T-bet |
| 基金项目:国际科技合作专项(编号:2013DFA30700) |
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| 中文摘要: |
| 目的:探讨黄芪糖蛋白对胶原诱导性关节炎(Collagen-induced Arthritis,CIA)小鼠特异性转录因子T-bet和GATA-3表达的影响,阐述黄芪糖蛋白治疗胶原诱导性关节炎小鼠的免疫作用机制。方法:建立牛Ⅱ型胶原诱导的小鼠关节炎模型,随机分为CIA模型组、氢化可的松阳性对照组、黄芪糖蛋白低剂量组、中剂量组、高剂量组;HE染色观察CIA小鼠脾组织损伤程度;采用流式细胞术检测CIA小鼠外周血IFN-γ和IL-4的水平;Western blot法检测CIA小鼠脾组织中T-bet和GATA-3蛋白的表达。结果:与模型组比较,黄芪糖蛋白改善了CIA小鼠脾组织损伤情况,减轻炎性反应细胞浸润,下调了外周血IFN-γ和IL-4水平(P<0.05);同时,降低了T-bet和GATA-3蛋白的表达(P<0.05)。结论:黄芪糖蛋白对CIA小鼠的治疗作用,可能是与降低T-bet、GATA-3表达,调整Th1/Th2功能失衡有关。 |
| English Summary: |
| To explore the effects of Astragalus glycoproteins on collagen-induced arthritis mice's specific transcription factors, T-bet and GATA-3, expression, and to clarify the immune mechanism of Astragalus glycoprotein on the treatment in collagen-induced arthritis mice. Methods:CIA model was induced by bovine Ⅱcollagen in mice. Mice were randomly divided into a CIA model group, a hydrocortisone positive control group, a Astragalus glycoprotein low dose group, a middle dose group and a high dose group. HE was used to observe the CIA mice spleen tissues damage. IFN-γ and IL-4 level were measured with flow cytometry in CIA mice. Western blot was used to analyze T-bet and GATA-3 protein expression. Results:Compared with the model group, Astragalus glycoprotein improved spleen tissue damage in CIA mice, and inhibited the infiltration of inflammatory cells. Astragalus glycoprotein reduced IFN-γand IL-4 level (P<0.05) and T-bet and GATA-3 protein expression (P<0.05). Conclusion:The mechanisms of action of Astragalus glycoprotein on CIA mice may be related to the decrease of T-bet and GATA-3 expression and function balance of the Th1 and Th2 cells. |
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