【摘要】：目的:研究強(qiáng)直性脊柱炎(ankylosing spondylitis,AS)患者體內(nèi)信號轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄活化蛋白3(signal transducer and activator of transcription 3,STAT3)的表達(dá)以及經(jīng)腫瘤壞死因子抑制劑(抗TNF-α)和非甾體抗炎藥(美洛昔康)治療前后STAT3水平的變化。分析STAT3與血沉(ESR)、C-反應(yīng)蛋白(CRP)、疾病活動指數(shù)(BASDAI)等指標(biāo)的相關(guān)性,探討AS的病因與STAT3基因的關(guān)聯(lián)性及兩種藥物治療AS與STAT3基因的相互關(guān)聯(lián)。方法:選取AS患者52例,隨機(jī)分為2組。各組分別接受抗TNF-α和美洛昔康藥物治療。另設(shè)健康對照組26例。評估各組性別、年齡、病程、HLA-B27、指地距、枕壁距、影像學(xué)得分以及治療前后晨僵、疼痛VAS評分、ESR、CRP、BASDAI等AS活動性指標(biāo)。采用酶聯(lián)免疫吸附法(ELISA)測定各組血清STAT3的表達(dá)水平,比較各組血清STAT3表達(dá)水平的統(tǒng)計學(xué)差異。結(jié)果:AS患者血清中STAT3的表達(dá)水平與健康對照組相比具有統(tǒng)計學(xué)意義(p0.01)抗TNF-α及美洛昔康治療后,AS患者的CRP、ESR、VAS、BASDAI等指標(biāo)均有改善;美洛昔康治療后AS患者血清中STAT3的表達(dá)水平與對照組相比具有統(tǒng)計學(xué)意義(p0.05);而抗TNF-α治療后AS患者血清中STAT3的表達(dá)水平與對照組相比沒有顯著的變化(p0.05)。結(jié)論:1.強(qiáng)直性脊柱炎患者血清STAT3明顯高于健康對照組,STAT3信號通路可能參與了AS的發(fā)病過程。2.AS患者經(jīng)TNF-α抑制劑治療后,血清STAT3水平?jīng)]有明顯的變化,TNF-α抑制劑對強(qiáng)直性脊柱炎的調(diào)控主要并非通過STAT3信號通路。3.AS患者經(jīng)非甾體抗炎藥物治療后,血清STAT3水平較治療前升高,提示STAT3信號通路可能調(diào)控了AS對NSAID敏感的獨立的炎癥過程。
[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- 偽) 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- 偽 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- 偽, 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- 偽 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- 偽 inhibitor, the level of serum STAT3 in patients with 2.AS did not change significantly. The regulation of TNF- 偽 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.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：R593.23

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