發(fā)布時(shí)間：2018-02-10 12:38

  本文關(guān)鍵詞： 血管內(nèi)皮生長(zhǎng)因子 血漿濃度 多態(tài)性 強(qiáng)直性脊柱炎　出處：《南京醫(yī)科大學(xué)》2017年博士論文　論文類型：學(xué)位論文

【摘要】：目的:強(qiáng)直性脊柱炎是一種自身免疫性炎癥性疾病,以腰痛,骶髂關(guān)節(jié)炎,和脊柱強(qiáng)直為臨床特點(diǎn)。強(qiáng)直性脊柱炎的發(fā)病機(jī)制尚不清楚,與血管生成和遺傳背景相關(guān)的各種生物標(biāo)志物在強(qiáng)直性脊柱炎在發(fā)病過程中起重要作用。血管內(nèi)皮生長(zhǎng)因子是一種促進(jìn)血管內(nèi)皮細(xì)胞遷移和增殖的血管生成因子,具有增加血管通透性和介導(dǎo)炎癥的作用。血管生成在多種風(fēng)濕性疾病,包括類風(fēng)濕關(guān)節(jié)炎,銀屑病性關(guān)節(jié)炎,強(qiáng)直性脊柱炎,系統(tǒng)性硬化癥中發(fā)揮作用,表明抑制血管生成可能是一個(gè)有用的治療方法。血管內(nèi)皮生長(zhǎng)因子是最有力的促血管生成分子,并導(dǎo)致強(qiáng)直性脊柱炎的血管生成。我們假設(shè),血管內(nèi)皮生長(zhǎng)因子多態(tài)性和血漿水平可能有助于強(qiáng)直性脊柱炎的易感性。方法:對(duì)強(qiáng)直性脊柱炎患者208例和412例住院其他患者對(duì)照組的病例對(duì)照研究,檢驗(yàn)強(qiáng)直性脊柱炎風(fēng)險(xiǎn)性,VEGF基因型,中國人群中血管內(nèi)皮生長(zhǎng)因子的血漿水平之間的關(guān)聯(lián)。使用基質(zhì)輔助激光解吸電離飛行時(shí)間質(zhì)譜進(jìn)行基因分型。對(duì)其中120例患者和120名對(duì)照組患者,使用酶聯(lián)免疫吸附測(cè)定法測(cè)定血漿VEGF濃度水平。結(jié)果:我們發(fā)現(xiàn),血管內(nèi)皮生長(zhǎng)因子rs3025039 C/T基因多態(tài)性增加強(qiáng)直性脊柱炎的患病風(fēng)險(xiǎn),在強(qiáng)直性脊柱炎患者組中,血管內(nèi)皮生長(zhǎng)因子的平均血漿濃度相比對(duì)照組顯著較高。在強(qiáng)直性脊柱炎患者組中,男性血管內(nèi)皮生長(zhǎng)因子水平明顯高于女性。分層后,rs3025039 CC基因型強(qiáng)直性脊柱炎患者的平均血漿濃度明顯高于對(duì)照組。血漿VEGF水平與年齡、HLA-B27、CRP或骶髂關(guān)節(jié)評(píng)分,在患者組和對(duì)照組之間沒有顯著差異。結(jié)論:這項(xiàng)研究證據(jù)表明,有可能血管內(nèi)皮生長(zhǎng)因子rs3025039多態(tài)性,血管內(nèi)皮生長(zhǎng)因子血漿濃度和強(qiáng)直性脊柱炎患病風(fēng)險(xiǎn)之間存在聯(lián)系。然而,我們的結(jié)果是從一個(gè)中等大小的樣品,因此這是一個(gè)初步的結(jié)論。需在一個(gè)更大和更多樣化的種族樣本中驗(yàn)證,以便確認(rèn)這些發(fā)現(xiàn)。
[Abstract]:Objective: ankylosing spondylitis is an autoimmune inflammatory disease characterized by lumbago sacroiliac arthritis and spinal ankylosis. Various biomarkers associated with angiogenesis and genetic background play an important role in the pathogenesis of ankylosing spondylitis. Vascular endothelial growth factor (VEGF) is an angiogenic factor that promotes the migration and proliferation of vascular endothelial cells. Angiogenesis plays a role in many rheumatoid diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, systemic sclerosis. This suggests that inhibition of angiogenesis may be a useful treatment. Vascular endothelial growth factor is the most potent angiogenic molecule and causes angiogenesis in ankylosing spondylitis. Vascular endothelial growth factor polymorphism and plasma levels may contribute to the susceptibility of ankylosing spondylitis. Methods: a case-control study was conducted in 208 patients with ankylosing spondylitis and 412 other hospitalized controls. To test the genotype of VEGF in the risk of ankylosing spondylitis, Association between plasma levels of vascular endothelial growth factor in Chinese population. Genotyping using matrix assisted laser desorption ionization time of flight mass spectrometry. 120 patients and 120 controls. Results: we found that the polymorphism of vascular endothelial growth factor (rs3025039) C / T gene increased the risk of ankylosing spondylitis in patients with ankylosing spondylitis. The average plasma concentration of vascular endothelial growth factor was significantly higher than that of the control group. After stratification, the mean plasma concentration of VEGF in male was significantly higher than that in female. The average plasma concentration in patients with ankylosing spondylitis genotype rs3025039CC was significantly higher than that in control group. The plasma VEGF level and age of HLA-B27C-CRP or sacroiliac joint score were significantly higher than those in control group. There was no significant difference between the patient group and the control group. Conclusion: the evidence in this study suggests the possibility of vascular endothelial growth factor rs3025039 polymorphism. There is a link between the plasma concentration of vascular endothelial growth factor and the risk of ankylosing spondylitis. So this is a preliminary conclusion. It needs to be tested in a larger and more diverse ethnic sample in order to confirm these findings.
【學(xué)位授予單位】：南京醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2017
【分類號(hào)】：R593.23

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相關(guān)期刊論文 前1條

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本文編號(hào)：1500530