骨桥蛋白在氟中毒肾损害发生机制中的作用

发布时间：2018-01-26 21:20

本文关键词： 氟中毒肾脏骨桥蛋白　出处：《吉林大学》2006年硕士论文　论文类型：学位论文

【摘要】： 肾脏作为氟的主要排泄器官,在氟中毒非骨相损害中越来越受到重视,有关氟中毒肾损害的文献日渐增多,但过量氟引起肾损害的机制迄今尚未完全阐明。本文在大鼠动物模型与体外肾小管上皮细胞培养相结合的基础上,应用形态学、免疫组织化学、生物化学、分子生物学、观察氟中毒肾损害的性质、特点着重探讨骨桥蛋白在肾损害发生发展中的作用。本文的主要结果和结论是:①不同钙营养状况、不同投氟时间和投氟剂量引起的肾脏病理改变不尽相同应用图象分析仪对肾小囊囊腔、肾小管管腔的面积及直径参数进行定量分析,发现在常食和偏食染氟组肾小囊腔均较对照组扩张明显;对皮髓质交界处的肾小管腔的等圆直径进行测量,染氟同等剂量和同样时间的情况下,偏食组较常食组扩张明显。②氟中毒肾损害的发生发展中有氧化应激参与,但氧化应激不象是始动环节或唯一机制。③氟中毒肾组织OPN的表达增强可能具有肾保护作用;OPN可在血清和尿中检出,故可能成为氟中毒肾损害的一种标志物。
[Abstract]:As the main excretory organ of fluoride, kidney is paid more and more attention in the fluorosis non-bone damage, and the literature about fluorosis kidney damage is increasing day by day. However, the mechanism of renal damage caused by excessive fluoride has not been fully elucidated. Based on the combination of rat model and renal tubular epithelial cell culture in vitro, morphology, immunohistochemistry and biochemistry were used. Molecular biology was used to observe the nature of renal damage caused by fluorosis. The role of osteopontin in the development of renal damage was discussed. The main results and conclusions were as follows: 1. The pathological changes of kidney caused by different fluorine time and dose were analyzed quantitatively by image analyzer in the area and diameter of renal microsac and tubule lumen. It was found that the dilatation of renal microsac was more obvious in the fluorine-exposed group than in the control group. The isodyclic diameters of the renal tubule cavity at the junction of the dermatomedullary were measured at the same dose and at the same time. Oxidative stress was involved in the occurrence and development of renal damage caused by fluorosis in the partial diet group compared with the normal diet group. 2. However, oxidative stress does not appear to be the initiator or the only mechanism. 3. The increased expression of OPN in renal tissue of fluorosis may have renal protective effect. OPN can be detected in serum and urine, so it may be a marker of renal damage caused by fluorosis.
【学位授予单位】：吉林大学
【学位级别】：硕士
【学位授予年份】：2006
【分类号】：R363

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