汞暴露所致小鼠肾毒性的实验研究  

Experimental study of mercury exposure-induced renal toxicity in mice

作　　者：黎丽 陈春帆 梁韬[3] 苏敏[4] 

机构地区：[1]环境监测站广西北流市环保局,广西北流547400 [2]环境监察大队广西北流市环保局,广西北流547400 [3]广西医科大学,广西南宁530021 [4]桂林医学院,广西桂林533000

出　　处：《四川生理科学杂志》2015年第1期10-13,共4页Sichuan Journal of Physiological Sciences

摘　　要：目的:研究氯化汞暴露对小鼠肾脏器官及生理功能的影响,并探讨其分子机制。方法:挑选健康雄性KM小鼠随机分为正常对照组(n=8)及低、中、高氯化汞染毒组(ig,1 mg·kg-1、5 mg·kg-1、10 mg·kg-1,n=8)。2周后,计算小鼠体重和肾脏指数变化,检测24 h尿蛋白含量和ELISA法检测血清TNF-α、IL-6的浓度。同时,应用Western blotting法测定肾脏组织内源性NF-κBp50表达。结果:与正常对照组比较,不同浓度的氯化汞染毒小鼠均出现明显的体重减轻和肾脏器官肿大(P<0.01),24 h尿蛋白含量明显升高(P<0.01),血清TNF-α、IL-6的浓度显著增高(P<0.01)。而肾脏组织NF-κBp50蛋白表达也显著上调(P<0.01)。结论:金属汞暴露明显诱导小鼠肾脏细胞发生毒性损伤,其机理可能与病理性炎症应激有关。Objective： To study the effects of mercury bichloride exposure on kidney tissue and physiological functions in mice, and to explore the molecular mechanism. Methods： Selection of healthy male KM mice were randomly divided into four groups., nor-real control group（n= 8） and the low, medium and high mercuric chloride-treated groups（ig, 1 mg kg-1, 5 mg · kg-1 10 mg ~ kg-1 · n=8）. At the end of 2 weeks, body mass and kidney index of mice were measured 24 h proteinuria content was de- tected, and serum concentrations of TNF-a, and IL-6 were determined using ELISA method in addition, endogenous NF-kBp50 ex- pression in the kidney was assessed by Western blotting assay. Results.. Compared with normal control, treatment with different con- centrations of mercuric chloride in mice showed marked weight loss and kidney enlargement（P〈0. 01） 24 h proteinuria concentration was significantly elevated（P〈0.01） serum TNF-a, IL-6 concentrations were inereased（P〈0.01） intrarenal NF-xBp50 protein ex- pression was also significantly upregulated（P〈0. 01）. Conclusions： Metallic mercury exposure significantly induced cytotoxicity in renal cells, which the mechanism may be related to development of pathological inflammatory stress.

关 键 词：氯化汞 肾毒性 炎症应激 

分 类 号：R285.5[医药卫生—中药学]