CCK-8对IL-1β诱导大鼠RSC-364细胞株增殖及p38MAPK磷酸化的影响

发布时间：2018-05-31 00:47

本文选题：类风湿性关节炎 + 滑膜细胞　；参考：《河北医科大学》2005年硕士论文

【摘要】：目的:类风湿性关节炎(rheumatoid arthritis, RA)是一种慢性炎症性自身免疫疾病,以持续性滑膜炎、滑膜组织增生和血管翳形成为特点,逐步侵袭软骨组织最终导致关节结构破坏和功能障碍。RA 的病因及发病机制尚未明了,近年来研究表明成纤维样滑膜细胞(fibroblast-like synoviocytes, FLS)在RA 的发病、慢性炎症的维持和骨与软骨的结构破坏等方面有着重要作用。RA 患者血清和关节液中异常升高的IL-1β促进滑膜组织活化和增生,IL-1β在RA FLS 信号转导中,可以瞬时导致蛋白质酪氨酸磷酸化的程度增加,并激活MAPK通路。MAPK 超家族是一组广泛分布于胞浆中具有丝氨酸和酪氨酸双重磷酸化能力的蛋白激酶,已证实其亚家族p38 MAPK 参与调控多种细胞增殖反应。八肽胆囊收缩素(cholecystokinin octapeptide, CCK-8)属于脑肠肽,具有免疫调节和抗炎作用,已有研究证实CCK-8 在TNF-α存在下可以抑制大鼠滑膜细胞株RSC-364 和胶原性关节炎(collagen-induced arthritis, CIA)大鼠滑膜细胞增殖。CCK-8 对IL-1β诱导的滑膜细胞增殖是否有调节作用还未见相关报道,为深入研究CCK-8 对治疗RA 的潜在作用及机理,本实验观察了CCK-8 对IL-1β诱导RSC-364 细胞增殖的影响,并对其作用机制进行了初步探讨。方法:1.四唑盐(MTT)比色法检测CCK-8 对IL-1β诱导
[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- 伪. 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
【学位授予单位】：河北医科大学
【学位级别】：硕士
【学位授予年份】：2005
【分类号】：R363

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