氯化汞所致肾病综合征及氧化损伤机制的实验研究  被引量:6

Experimental study on the mechanism of nephrotic syndrome and oxidative damage caused by mercuric chloride

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作  者:孙琳 李侠[2] 赵玉军[2] 郑熠娇 尚磊[2] SUN Lin;LI Xia;ZHAO Yu-jun;ZHENG Yi-Jiao;SHANG Lei(School of Medicine and Life Sciences,University of Jinan-Shandong Academy of Medical Sciences,Jinan 250062,China)

机构地区:[1]济南大学山东省医学科学院医学与生命科学学院,山东济南250062 [2]山东省职业卫生与职业病防治研究院山东第一医科大学(山东省医学科学院),山东济南250062

出  处:《工业卫生与职业病》2020年第3期230-235,共6页Industrial Health and Occupational Diseases

基  金:山东省医学科学院院级科技计划(2017-28);山东省医药卫生科技发展计划项目(2017WS711,2018WS171)。

摘  要:目的探究汞致肾病综合征大鼠肾脏损伤与氧化应激的关系,为汞致肾病综合征发病机制的研究提供实验基础。方法将BN大鼠48只随机分成对照组、染毒组。对照组注射NaCl,染毒组分别于第1、3、5、7、11、第13天以1mg/kg腹部皮下注射HgCl2(1mg/ml)造模。实验期间进行尿蛋白、血生化、血汞、尿汞等指标监测,于第14、21、28、第35天处死部分大鼠,观察病理学变化,进行肾组织还原性谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-PX)、超氧化物歧化酶(SOD)及丙二醛(MDA)检测。结果与对照组比较,染毒组表现出体内汞含量升高;蛋白尿,低蛋白血症,高脂血症,肾组织GSH及MDA升高,GSH-PX、SOD活力下降,氧化-抗氧化系统失衡等症状,病理可见肾小球基质增多、肾小管扩张、肾小管蛋白管型等变化,其中第28天或第35天病变程度严重。结论在无机汞导致肾病综合征的发病机制中,汞导致的氧化应激可能是汞致肾损伤的重要原因。抑制汞导致的氧化应激可作为对症治疗和抑制免疫与炎症反应之外的新思路。Objective To investigate the relationship between renal injury and oxidative stress in rats with nephrotic syndrome caused by mercury,and to provide experimental basis for the study of the pathogenesis of nephrotic syndrome caused by mercury.Methods 48Brown-Norway rats were randomly divided into control group and exposure group.The control group was injected with Nacl,and the exposed group was subcutaneously injected with HgCl2(1mg/ml)on the 1st,3rd,5th,7th,11th,and 13th day,respectively.During the experiment,urine protein,blood biochemistry,blood mercury,urinary mercury and other indicators were monitored.Some rats were sacrificed on days 14,21,28,and 35,and pathological changes were observed to reduce renal glutathione(GSH).Glutathione peroxidase(GSH-PX),superoxide dismutase(SOD)and malondialdehyde(MDA)were detected.Results Compared with the control group,the exposed group showed elevated mercury levels in the body;proteinuria,hypoproteinemia;hyperlipidemia;elevated GSH and MDA in renal tissues,decreased activity of GSH-PX and SOD,and oxidation-resistance Symptoms such as imbalance of the oxidative system,pathological changes such as increased glomerular matrix,tubular dilatation,and tubular protein tube type,the most severe lesions on the 28th or 35th day.Conclusions In the pathogenesis of nephrotic syndrome caused by inorganic mercury,oxidative stress caused by mercury may be an important cause of mercury-induced renal damage.The inhibition of oxidative stress caused by mercury can be used as a new idea in symptomatic treatment and inhibition of immune and inflammatory responses.

关 键 词:汞中毒 肾病综合征 机制研究 

分 类 号:R135.13[医药卫生—劳动卫生]

 

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