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链脲佐菌素诱导的糖尿病大鼠多形核白细胞膜流动性降低

Decreased fluidity of polymorphonuclear leukocyte membrane in streptozocin-induced diabetic rats.

作者信息

Masuda M, Murakami T, Egawa H, Murata K

机构信息

Department of Clinico-Laboratory Medicine, Kansai Medical University, Osaka, Japan.

出版信息

Diabetes. 1990 Apr;39(4):466-70. doi: 10.2337/diab.39.4.466.

DOI:10.2337/diab.39.4.466
PMID:2138577
Abstract

Using flow cytometry with the excimer-forming lipid technique with pyrenedecanoic acid, we measured membrane fluidity of polymorphonuclear leukocytes (PMNs) from 20 streptozocin (STZ)-induced diabetic rats. Diabetes mellitus was induced in male Sprague-Dawley rats (body wt 243 +/- 11 g) with an injection of 25 mg/kg i.v. STZ. Membrane fluidity of PMNs was significantly lower at 2 wk after the STZ injection when serum glucose reached the plateau (31.1 +/- 5.8 mM), and after 3 wk, membrane fluidity remained unchanged. In 7 STZ-resistant rats for which serum glucose was less than 10 mM at 2 wk after the STZ injection, gradual normalization in membrane fluidity was observed. PMN membrane fluidity at each week correlated inversely with respective serum glucose levels 1 wk previously (r = -0.76) but not with serum lipid levels. Cross-incubation studies ascribed this observation to factors in the diabetic rat serum. Glycosylated protein, which was separated from diabetic rat serum, decreased membrane fluidity of control rat PMNs. Human diabetic subjects have an increased risk for infection, which may be due partly to altered membrane fluidity of their PMNs.

摘要

我们采用结合了芘癸酸的准分子形成脂质技术的流式细胞术,测量了20只链脲佐菌素(STZ)诱导的糖尿病大鼠的多形核白细胞(PMN)的膜流动性。对雄性Sprague-Dawley大鼠(体重243±11 g)静脉注射25 mg/kg STZ诱导糖尿病。在STZ注射后2周,当血清葡萄糖达到平台期(31.1±5.8 mM)时,PMN的膜流动性显著降低,3周后,膜流动性保持不变。在7只STZ抵抗大鼠中,STZ注射后2周血清葡萄糖低于10 mM,观察到膜流动性逐渐恢复正常。每周的PMN膜流动性与前1周各自的血清葡萄糖水平呈负相关(r = -0.76),但与血清脂质水平无关。交叉孵育研究将这一观察结果归因于糖尿病大鼠血清中的因素。从糖尿病大鼠血清中分离出的糖基化蛋白降低了对照大鼠PMN的膜流动性。人类糖尿病患者感染风险增加,这可能部分归因于其PMN膜流动性的改变。

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