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链脲佐菌素诱导糖尿病对自然发生牙龈炎大鼠白细胞功能的影响。

The effect of leukocyte function of streptozotocin-induced diabetes in naturally occurring gingivitis rat.

作者信息

Inoue H, Shinohara M, Ohura K

机构信息

Department of Pharmacology, Osaka Dental University, Japan.

出版信息

J Osaka Dent Univ. 1997 Dec;31(1-2):47-54.

PMID:9872087
Abstract

Although diabetes mellitus is known to aggravate periodontal disease, the precise relationship between these two entities is far from being completely understood. Further study of this relationship was therefore undertaken in the form of observation of both naturally occurring gingivitis in rats (ODUS/Odu) and effects produced by induction of experimental diabetes mellitus by injection of streptozotocin (STZ: 65 mg/kg, i.v.). At one and 3 mon after STZ injection, liquid paraffin was injected intraperitoneally. Four days thereafter, pocket probing depths of rats were measured and blood samples as well as peritoneal macrophages were collected from both experimental animals and non diabetic controls. Both chemotaxis and phagocytosis of macrophages were studied. At one and 3 mon after STZ injection, pocket probing depths of diabetic animals were significantly deeper than those of controls (p < 0.001). Pocket probing depths were deeper at 3 mon after STZ injection than after 1 mon in diabetic animals. At three months after STZ injection, there was a high degree of positive correlation between pocket probing depths, blood glucose levels, triglyceride, and hemoglobin A1c levels (p < 0.01). Also, macrophage chemotaxis was more suppressed in diabetic rats than it was in controls. Additionally, both phagocytosis ratios and phagocytosis indices of macrophages in the diabetes group were significantly more suppressed than those in controls in both experimental periods (p < 0.001). Findings suggest that both chemotaxis and phagocytosis are compromised in macrophages from rats rendered diabetic by STZ injection. Thus as host defense mechanisms become weakened, there is a corresponding progression of periodontal disease.

摘要

尽管已知糖尿病会加重牙周疾病,但这两种疾病的确切关系远未被完全理解。因此,以观察大鼠自然发生的牙龈炎(ODUS/Odu)以及注射链脲佐菌素(STZ:65 mg/kg,静脉注射)诱导实验性糖尿病所产生的影响的形式,对这种关系进行了进一步研究。在注射STZ后1个月和3个月,腹腔注射液体石蜡。此后4天,测量大鼠的牙周袋探诊深度,并从实验动物和非糖尿病对照中采集血样以及腹腔巨噬细胞。研究了巨噬细胞的趋化性和吞噬作用。在注射STZ后1个月和3个月,糖尿病动物的牙周袋探诊深度明显深于对照组(p < 0.001)。在糖尿病动物中,注射STZ后3个月的牙周袋探诊深度比1个月后更深。在注射STZ后3个月,牙周袋探诊深度、血糖水平、甘油三酯和糖化血红蛋白A1c水平之间存在高度正相关(p < 0.01)。此外,糖尿病大鼠的巨噬细胞趋化性比对照组更受抑制。另外,在两个实验阶段,糖尿病组巨噬细胞的吞噬率和吞噬指数均明显低于对照组(p < 0.001)。研究结果表明,注射STZ致糖尿病大鼠的巨噬细胞趋化性和吞噬作用均受损。因此,随着宿主防御机制减弱,牙周疾病会相应进展。

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