本文選題：類風(fēng)濕性關(guān)節(jié)炎 + 滑膜細(xì)胞��； 參考：《河北醫(yī)科大學(xué)》2005年碩士論文

【摘要】：目的:類風(fēng)濕性關(guān)節(jié)炎(rheumatoid arthritis, RA)是一種慢性炎癥性自身免疫疾病,以持續(xù)性滑膜炎、滑膜組織增生和血管翳形成為特點,逐步侵襲軟骨組織最終導(dǎo)致關(guān)節(jié)結(jié)構(gòu)破壞和功能障礙。RA 的病因及發(fā)病機制尚未明了,近年來研究表明成纖維樣滑膜細(xì)胞(fibroblast-like synoviocytes, FLS)在RA 的發(fā)病、慢性炎癥的維持和骨與軟骨的結(jié)構(gòu)破壞等方面有著重要作用。RA 患者血清和關(guān)節(jié)液中異常升高的IL-1β促進(jìn)滑膜組織活化和增生,IL-1β在RA FLS 信號轉(zhuǎn)導(dǎo)中,可以瞬時導(dǎo)致蛋白質(zhì)酪氨酸磷酸化的程度增加,并激活MAPK通路。MAPK 超家族是一組廣泛分布于胞漿中具有絲氨酸和酪氨酸雙重磷酸化能力的蛋白激酶,已證實其亞家族p38 MAPK 參與調(diào)控多種細(xì)胞增殖反應(yīng)。八肽膽囊收縮素(cholecystokinin octapeptide, CCK-8)屬于腦腸肽,具有免疫調(diào)節(jié)和抗炎作用,已有研究證實CCK-8 在TNF-α存在下可以抑制大鼠滑膜細(xì)胞株RSC-364 和膠原性關(guān)節(jié)炎(collagen-induced arthritis, CIA)大鼠滑膜細(xì)胞增殖。CCK-8 對IL-1β誘導(dǎo)的滑膜細(xì)胞增殖是否有調(diào)節(jié)作用還未見相關(guān)報道,為深入研究CCK-8 對治療RA 的潛在作用及機理,本實驗觀察了CCK-8 對IL-1β誘導(dǎo)RSC-364 細(xì)胞增殖的影響,并對其作用機制進(jìn)行了初步探討。 方法:1.四唑鹽(MTT)比色法檢測CCK-8 對IL-1β誘導(dǎo)
[Abstract]:Objective: rheumatoid arthritis (RAA) is a chronic inflammatory autoimmune disease characterized by persistent synovitis, synovial hyperplasia and pannus formation. The etiology and pathogenesis of progressive invasion of chondrocytes leading to destruction of articular structure and dysfunction of function .RA have not been clarified in recent years. Recent studies have shown that fibroblast-like synoviocytes (FLSs) occur in RA. The maintenance of chronic inflammation and the structural destruction of bone and cartilage play an important role. The abnormal elevation of IL-1 尾 in serum and articular fluid of RA patients promotes the activation of synovial tissue and proliferation of IL-1 尾 in RA FLS signal transduction. MAPK superfamily is a group of protein kinases widely distributed in the cytoplasm with the ability of both serine and tyrosine phosphorylation. It has been proved that its subfamily p38 MAPK is involved in the regulation of multiple cell proliferation responses. Cholecystokinin octapeptide (CCK-8) is a brain intestinal peptide with immunomodulatory and anti-inflammatory effects. It has been proved that CCK-8 can inhibit the proliferation of synovial cell line RSC-364 and collagen-induced arthritis (CIAA) in the presence of TNF- 偽. Whether CCK-8 can regulate the proliferation of synovial cells induced by IL-1 尾 has not been reported. In order to study the potential role and mechanism of CCK-8 in the treatment of RA, the effect of CCK-8 on the proliferation of RSC-364 cells induced by IL-1 尾 was observed and its mechanism was preliminarily discussed. Method 1: 1. Detection of IL-1 尾 induced by CCK-8 by MTT colorimetry
【學(xué)位授予單位】：河北醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2005
【分類號】：R363

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