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目的研究贫铀摄入后不同时相点对大鼠肾脏的损伤效应。方法雄性Wistar大鼠40只,其中20只以含有50μg/L和70μg/kg的贫铀饮水及饲料喂食大鼠作为摄入组。观察大鼠接触贫铀后3、6、12、18个月大鼠肾脏超微结构和病理形态学改变,肾功能检测和胶原染色,并采用免疫荧光和蛋白印记杂交检测肾脏不同时间段纤维化相关因子TGF-β1、Smad、TIMP和MMP-9表达。结果大鼠摄入贫铀后不同时间段大鼠肾脏出现不同程度的病理改变,表现为肾小球固缩、后继肾小管萎缩和局部肾间质纤维组织增生以及炎性细胞浸润。纤维化程度随接触时间延长而加重。胶原染色显示胶原分布主要位于肾小管周围,且具有区域性。Western blot分析显示贫铀接触后大鼠肾脏中TGF-β1等纤维化相关因子蛋白含量均有不同程度的增加(P<0.05)。结论贫铀长时间暴露后大鼠肾脏可出现病理学及超微结构的改变,TGF-β1、Smad、TIMP和MMP-9均参与了其纤维化进程。
Objective To study the effect of depleted uranium on rat kidney injury at different time points after ingestion. Methods Forty male Wistar rats, of which 20 were fed with depleted uranium drinking water containing 50μg / L and 70μg / kg diet and feed. The renal ultrastructures, pathological changes, renal function tests and collagen staining were observed at 3, 6, 12 and 18 months after exposure to depleted uranium in rats. Fibrosis was detected by immunofluorescence and Western blotting at different time points Factors TGF-β1, Smad, TIMP and MMP-9 expression. Results The pathological changes of rats’ kidneys were observed at different time points after depleted uranium in rats. Glomerular pyknosis, subsequent tubular atrophy and local interstitial fibrosis and inflammatory cell infiltration were observed. The degree of fibrosis aggravated with prolonged exposure. Collagen staining showed that the collagen distribution was mainly located around the tubules and was regional. Western blot analysis showed that TGF-β1 and other fibrosis-related protein levels in the kidney of rats after exposure to depleted uranium increased to some extent (P <0.05). Conclusion Pathological and ultrastructural changes may occur in rat kidney after lean uranium exposure for a long time. TGF-β1, Smad, TIMP and MMP-9 are all involved in the process of fibrosis.