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作 者:陈吉[1] 高美丽[1] 白晓茹[1] 崔宏[1] 王觅柱
机构地区:[1]内蒙古医学院第三附属医院消化科,内蒙古自治区包头市014010 [2]包头市医学院第二附属医院消化科,内蒙古自治区包头市014010
出 处:《世界华人消化杂志》2009年第2期209-212,共4页World Chinese Journal of Digestology
摘 要:目的:探讨溃疡性结肠炎(ulcerative colitis,UC)患者肠黏膜活检组织中NF-κB的表达及其与细胞因子水平的关系.方法:用免疫组化SP方法检测60例活动期UC内镜活检标本及30例正常对照石蜡组织中NF-κB表达情况,同时用放免法检测UC组和正常对照组血清中IL-1β,TNF-α和IL-10的表达水平.结果:60例UC组中NF-κBp65均为阳性表达,主要分布在结肠黏膜上皮细胞、腺上皮细胞和巨噬细胞.对照组均为阴性和弱阳性表达,主要分布于上皮细胞.UC组的NF-κBp65表达平均灰度值与正常对照组比较差异有显著性(166.62±14.88vs142.30±19.01,P<0.05);活动期UC组血清中IL-1β、TNF-α表达水平显著高于正常对照组(1.29±0.36vs1.29±0.36,4.47±1.08vs1.37±0.26,均P<0.01),而IL-10表达水平二组间差异无统计学意义.NF-κBp65的表达与活动期UC病情活动性及内镜分级有相关性(P<0.05或0.01).结论:NF-κB诱导、参与了UC的发生、发展过程,并与UC病情活动性及内镜分级有较好相关性,可客观反应UC的炎症活动情况;促炎细胞因子IL-1β、TNF-α与抑炎性细胞因子IL-10的表达水平不一致,可能与NF-κB诱导调控有直接关系.AIM: To investigate the expressions of nuclear factor-KappaB (NF-KB), interleukin-1β (IL- 1β), tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10), and to explore the role of those molecules in ulcerative colitis (UC). METHODS: Thirty outpatients were taken as controls and 60 patients with active UC were recruited after colonscopy. The expression of NF- kB in colonic tissues was detected by immunohistochemistry. The serum concentration of IL- 1β, TNF-α and IL-10 were also measured. RESULTS: NF-kB p65 was positively expressed in all the tissues, mainly in epithelial cells, and also inflammatory cells in lamina propria, while it was negatively expressed or weakly positive in controls, mainly in epithelial cells. Their expression was significantly higher in UC tissues than in controls (166.62 ± 14.88 vs 142.30 ± 19.01, P 〈 0.05). The concentrations of IL-1β and TNF-α were significantly higher in active UC patients than in controls (1.29 ± 0.36 vs 1.29 ± 0.36, 4.47 ± 1.08 vs 1.37 ± 0.26, both P 〈 0.01). The expression of NF-kB p65 was related to active grade and endoscopic classification (P 〈 0.05 or 0.01). CONCLUSION: The expression of NF-kB and cytokines may be involved in the pathogenesis of UC, and their levels reflect the disease activity in UC. The expression of preinflammatory cytokines may be modulated by NF-kB.
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