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作 者:党胜春[1] 冯舒[1] 王平江[1] 沈耀[1] 张建新[1]
机构地区:[1]江苏大学附属医院普外科, 江苏省镇江212001
出 处:《中华急诊医学杂志》2014年第7期765-769,共5页Chinese Journal of Emergency Medicine
基 金:国家自然科学基金(81070287);江苏省自然科学基金(BK2011484、BK2012704)
摘 要:目的 探讨巨噬细胞(Mφ)表型在重症急性胰腺炎(severe acute pancreatitis,SAP)急性肾损伤中的机制.方法 雄性Wistar大鼠64只,随机(随机数字法)分为对照组(SO组)和SAP组,每组32只,采用逆行胰胆管注射5%牛磺胆酸钠制备SAP大鼠模型,于造模后2、6、12及24h分别取血和肾组织.自动生化分析仪测定血液中尿素氮(BUN)、肌酐(Cr)的改变.逆转录-聚合酶链反应(RT-PCR)方法检测肾组织IL-12、TNF-α、IL-10及TGF-β的mRNA的表达水平.蛋白质印迹法检测CD68、iNOS、Arg-1的表达.结果 SAP组各时点BUN、Cr的浓度均高于对照组(P <0.01,P<0.05);SAP组各时点肾组织IL-12、TNF-α、IL-10、TGF-β的mRNA的表达水平较对照组显著增高,差异具有统计学意义(P<0.01,P<0.05); SAP组各时点CD68、iNOS、Arg-1表达量均高于对照组.结论 SAP时炎症反应及炎症失衡是急性肾损伤的可能病理因素.Objective To investigate the macrophages (Mφ) phenotype mechanism in acute kidney injury caused by severe acute pancreatitis (SAP).Methods Sixty-four male Wistar rats were randomly divided into control group (SO) and SAP group (n =32 in each group).SAP rat model was made by retrograde cholangiopancreatic injection of 5% sodium taurocholate.At 2,6,12 and 24 h after modeling,the samples of blood and kidney tissue were collected.The levels of blood urea nitrogen (BUN) and creatinine (Cr) were detected by using automatic biochemical analyzer.The expressions of IL-12,TNF-α,IL-10 and TGF-β mRNA of kidney tissue were detected by fluorescence quantitative polymerase chain reaction (QRT-PCR).The levels of CD68,iNOS and Arg-1 were measured by Western blot.Results In the SAP group at each interval,BUN and Cr concentrations were significantly higher than those of the control group (P < 0.01,P < 0.05) ; Compared with the control group,the expressions of IL-12,TNF-α,IL-10 and TGF-β mRNA in renal tissue of SAP group were significantly higher (P < 0.01,P < 0.05).In the SAP group,the levels of CD68,iNOS and Arg-1 were higher than those in the control group.Conclusions Inflammation and inflammatory imbalances may be pathological factors of acute kidney injury following SAP.
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