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炎症性肠病中结肠和直肠黏蛋白的硫酸化:溃疡性结肠炎中直肠黏液硫酸化减少。

Sulphation of colonic and rectal mucin in inflammatory bowel disease: reduced sulphation of rectal mucus in ulcerative colitis.

作者信息

Raouf A H, Tsai H H, Parker N, Hoffman J, Walker R J, Rhodes J M

机构信息

University Department of Medicine, Liverpool, U.K.

出版信息

Clin Sci (Lond). 1992 Nov;83(5):623-6. doi: 10.1042/cs0830623.

Abstract
  1. Normal colonic mucin is heavily sulphated and this increases its resistance to degradation by bacterial enzymes. Any defect in mucus sulphation could therefore be important in the pathogenesis of ulcerative colitis. 2. Rectal biopsies taken at colonoscopy from patients with ulcerative colitis (n = 9), patients with Crohn's disease (n = 6) and control subjects (n = 16) were cultured for 24 h in the presence of N-[3H]acetylglucosamine and [35S]sulphate. Mucin was then extracted and purified, and the ratio of [35S]sulphate to N-[3H]acetylglucosamine incorporated into pure mucin was assessed. 3. The ratio of [35S]sulphate to N-[3H]acetylglucosamine incorporated into mucin was significantly reduced in rectal biopsies taken from patients with ulcerative colitis (0.463, 0.305-0.703, geometric mean and 95% confidence intervals) compared with control subjects (0.857, 0.959-1.111, P < 0.01). In patients with Crohn's disease the reduction in this ratio (0.559, 0.378-0.829) did not quite reach statistical significance (P = 0.06). There was no difference between the ratio of [35S]sulphate to N-[3H]acetylglucosamine incorporated into mucin in Crohn's disease and that in ulcerative colitis (P = 0.26). 4. In control subjects the ratio of [35S]sulphate to N-[3H]acetylglucosamine incorporated into mucin was higher in the rectal biopsies (0.882, 0.618-1.022) than in their paired proximal colonic biopsies (0.602, 0.421-0.861; P < 0.01), but this regional variation was not observed in either ulcerative colitis (rectum: 0.450, 0.262-0.773; right colon: 0.470, 0.321-0.690, P = 0.3) or Crohn's disease (rectum: 0.459, 0.260-0.815; right colon: 0.492, 0.260-0.929, P = 0.8).(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 正常结肠黏蛋白高度硫酸化,这增强了其对细菌酶降解的抵抗力。因此,黏液硫酸化的任何缺陷在溃疡性结肠炎的发病机制中可能都很重要。2. 对溃疡性结肠炎患者(n = 9)、克罗恩病患者(n = 6)和对照受试者(n = 16)在结肠镜检查时取的直肠活检组织,在N-[3H]乙酰葡糖胺和[35S]硫酸盐存在的情况下培养24小时。然后提取并纯化黏蛋白,并评估掺入纯黏蛋白中的[35S]硫酸盐与N-[3H]乙酰葡糖胺的比例。3. 与对照受试者(0.857,0.959 - 1.111,P < 0.01)相比,溃疡性结肠炎患者直肠活检组织中掺入黏蛋白的[35S]硫酸盐与N-[3H]乙酰葡糖胺的比例显著降低(0.463,0.305 - 0.703,几何均值和95%置信区间)。克罗恩病患者该比例的降低(0.559,0.378 - 0.829)未达到统计学显著性(P = 0.06)。克罗恩病患者与溃疡性结肠炎患者掺入黏蛋白的[35S]硫酸盐与N-[3H]乙酰葡糖胺的比例之间无差异(P = 0.26)。4. 在对照受试者中,直肠活检组织中掺入黏蛋白的[35S]硫酸盐与N-[3H]乙酰葡糖胺的比例(0.882,0.618 - 1.022)高于其配对的近端结肠活检组织(0.602,0.421 - 0.861;P < 0.01),但在溃疡性结肠炎(直肠:0.450,0.262 - 0.773;右结肠:0.470,0.321 - 0.690,P = 0.3)或克罗恩病(直肠:0.459,0.260 - 0.815;右结肠:0.492,0.260 - 0.929,P = 0.8)中均未观察到这种区域差异。(摘要截断于250字)

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