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作 者:刘刚[1] 侯良绢[2] LIU Gang;HOU Liang-juan(Department of lnfectious Disease,Chongqing Three Gorges Central Hospital,Chongqing 404000,China)
机构地区:[1]重庆三峡中心医院感染科,重庆404000 [2]重庆三峡医药高等专科学校解剖教研室,重庆404120
出 处:《中国生物制品学杂志》2019年第1期36-39,45,共5页Chinese Journal of Biologicals
摘 要:目的探讨睡眠剥夺(sleep deprivation,SD)对小鼠肾组织中炎症因子IL-6和TNF-α表达的影响。方法将C57雄性小鼠随机分为空白对照组及SD 24、48和72 h组,利用COBAS INTEGRA 800全自动生化分析仪检测小鼠血清中尿素氮(urea nitrogen,BUN),肌酐(creatinine,CREA)和尿酸(uric acid,URCA)的含量;黄嘌呤氧化酶法检测肾脏组织中超氧化物歧化酶(superoxide dismutase,SOD)活性,硫代巴比妥酸法检测丙二醛(malonaldehyde,MDA)含量;对动物进行组织学检查,ELISA法检测肾脏组织中IL-6和TNF-α含量。结果与空白对照组比较,随SD时间延长,小鼠血清中BUN、CREA和URCA含量在SD 24 h后显著增高(P <0. 01),48和72 h持续增高(P <0. 01);小鼠肾脏组织中SOD活性随SD时间延长持续下降(P <0. 01),MDA含量持续增加(P <0. 01);HE染色可见肾小管上皮细胞空泡样变性、轻度水肿,肾小球和间质内可见炎症细胞浸润和红细胞,肾小囊腔闭塞;IL-6、TNF-α含量随SD时间延长持续增加(P <0. 01)。结论 SD诱发肾组织氧化损伤,引起脂质过氧化,使得肾脏结构和功能受损,促进炎症因子IL-6和TNF-α的大量释放,激活炎症反应,加重对肾脏的损伤。Objective To investigate the effect of sleep deprivation on expressions of IL-6 and TNF-α in kidney of mice.Methods Male C57 mice were randomly divided into four groups.The mice in three test groups were subjected to deprivation for 24,48 and 72 h respectively,while those in control group were untreated.The urea nitrogen(BUN),creatinine(CREA) and uric acid(URCA) levels in sera of mice were determined by automatic biochemical analyzer,while the activity of superoxide dismutase(SOD) in renal tissue by xanthine oxidase method,and the malondialdehyde(MDA) content by thiobarbituric acid method.The histological features of renal tissue was analyzed by H&E staining.The expression levels of IL-6 and TNF-α in renal tissue was determined by ELISA.Results Compared with those in control group,with the increasing time for SD,the BUN,CREA and URCA contents in sera of mice increased significantly 24 h(P< 0.01)and continued to increase 48 and 72 h after SD(P< 0.01),while the SOD activity in renal tissue decreased continuously(P< 0.01),and the MDA content increased continuously(P< 0.01).HE staining showed vacuolar degeneration of renal tubular epithelial cells,mild edema,glomerular and interstitial inflammatory cell infiltration and visible red blood cells,as well as renal capsule obliteration.However,the IL-6 and TNF-α contents increased continuously with the increasing time for SD(P< 0.01).Conclusion SD induced the oxidative damage of renal tissues which elevated lipid peroxidation and impaired the structure and function of kidney.Massive release of inflammatory cytokines IL-6 and TNF-α activated the inflammatory responses which may further to contribute to kidney damage.
关 键 词:睡眠剥夺 炎症因子 氧化应激 肾脏 小鼠 IL-6 TNF-Α
分 类 号:R163[医药卫生—公共卫生与预防医学]
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