强直性脊柱炎STAT3表达及其与治疗的相关性研究

发布时间：2018-11-11 17:02

【摘要】：目的:研究强直性脊柱炎(ankylosing spondylitis,AS)患者体内信号转导和转录活化蛋白3(signal transducer and activator of transcription 3,STAT3)的表达以及经肿瘤坏死因子抑制剂(抗TNF-α)和非甾体抗炎药(美洛昔康)治疗前后STAT3水平的变化。分析STAT3与血沉(ESR)、C-反应蛋白(CRP)、疾病活动指数(BASDAI)等指标的相关性,探讨AS的病因与STAT3基因的关联性及两种药物治疗AS与STAT3基因的相互关联。方法:选取AS患者52例,随机分为2组。各组分别接受抗TNF-α和美洛昔康药物治疗。另设健康对照组26例。评估各组性别、年龄、病程、HLA-B27、指地距、枕壁距、影像学得分以及治疗前后晨僵、疼痛VAS评分、ESR、CRP、BASDAI等AS活动性指标。采用酶联免疫吸附法(ELISA)测定各组血清STAT3的表达水平,比较各组血清STAT3表达水平的统计学差异。结果:AS患者血清中STAT3的表达水平与健康对照组相比具有统计学意义(p0.01)抗TNF-α及美洛昔康治疗后,AS患者的CRP、ESR、VAS、BASDAI等指标均有改善;美洛昔康治疗后AS患者血清中STAT3的表达水平与对照组相比具有统计学意义(p0.05);而抗TNF-α治疗后AS患者血清中STAT3的表达水平与对照组相比没有显著的变化(p0.05)。结论:1.强直性脊柱炎患者血清STAT3明显高于健康对照组,STAT3信号通路可能参与了AS的发病过程。2.AS患者经TNF-α抑制剂治疗后,血清STAT3水平没有明显的变化,TNF-α抑制剂对强直性脊柱炎的调控主要并非通过STAT3信号通路。3.AS患者经非甾体抗炎药物治疗后,血清STAT3水平较治疗前升高,提示STAT3信号通路可能调控了AS对NSAID敏感的独立的炎症过程。
[Abstract]:Objective: to study signal transduction and transcription activating protein 3 (signal transducer and activator of transcription 3 in patients with ankylosing spondylitis (ankylosing spondylitis,AS). The expression of STAT3 and the changes of STAT3 level before and after treatment with tumor necrosis factor inhibitor (TNF- 伪) and nonsteroidal anti-inflammatory drug (meloxicam). To analyze the correlation between STAT3 and ESR (ESR), C-reactive protein (CRP), disease activity index (BASDAI), and to explore the relationship between the etiology of AS and STAT3 gene, and the correlation between AS and STAT3 gene in two kinds of drugs. Methods: 52 patients with AS were randomly divided into 2 groups. Each group was treated with anti TNF- 伪 and meloxicam respectively. In addition, 26 cases of healthy control group were set up. Sex, age, course of disease, HLA-B27, digital distance, occipital wall distance, imaging score, morning stiffness, VAS score of pain, ESR,CRP,BASDAI and so on were evaluated. The expression level of serum STAT3 was measured by Elisa (ELISA), and the statistical difference of serum STAT3 expression in each group was compared. Results: compared with the healthy control group, the expression of STAT3 in the serum of AS patients was significantly higher than that of the control group (p0.01). After treatment with meloxicam and anti-TNF- 伪, the CRP,ESR,VAS,BASDAI of AS patients was improved. The expression of STAT3 in serum of AS patients after meloxicam treatment was significantly higher than that of control group (p0.05), but the expression of STAT3 in AS patients after anti-TNF- 伪 treatment had no significant change compared with the control group (p0.05). Conclusion: 1. Serum STAT3 in patients with ankylosing spondylitis was significantly higher than that in healthy controls, and STAT3 signaling pathway might be involved in the pathogenesis of AS. After treatment with TNF- 伪 inhibitor, the level of serum STAT3 in patients with 2.AS did not change significantly. The regulation of TNF- 伪 inhibitor on ankylosing spondylitis is not mainly through STAT3 signaling pathway. After treatment with NSAIDs, the serum STAT3 level in 3.AS patients is higher than that before treatment. The results suggest that the STAT3 signaling pathway may regulate the independent inflammatory process of AS sensitive to NSAID.
【学位授予单位】：苏州大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R593.23

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