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作 者:董振超[1] 王坚[1] 王小红[1] 孔恩军 潘新梅 王颖[1] 郜黎伟[1] 林翼金 DONG Zhenchao WANG Jian WANG Xiaohong et al(Department of Emergency, People's Hospital of Dan yang , Dan yang 212300, CHINA)
出 处:《江苏医药》2016年第20期2189-2192,F0002,共5页Jiangsu Medical Journal
基 金:镇江市2013年度科技支撑计划(社会发展)指导性项目(FZ2013006)
摘 要:目的研究肾康注射液对大鼠重症急性胰腺炎(SAP)肾损伤的治疗作用。方法 90只雄性大鼠随机均分为三组。SAP组和肾康注射液治疗组构建大鼠SAP并发肾损伤模型。建模成功后3h,肾康注射液治疗组和正常对照组分别腹腔注射肾康注射液9ml/kg和生理盐水2ml/kg,每12小时注射1次。三组分别于给药后3、12、24h各处死10只大鼠,检测血清淀粉酶(AMY)、肌酐及尿素氮(BUN)水平,观察胰腺及肾组织光镜下病理学变化,采用实时定量聚合酶链反应法检测大鼠肾组织核因子NF-κB p65、TNF-α、IL-6及IL-10mRNA的表达。结果与SAP组比较,肾康注射液治疗组12h和24h的血清AMY、肌酐及BUN水平、胰腺组织及肾组织病理学评分以及肾组织NF-κB p65、TNF-α及IL-6mRNA表达水平均降低(P<0.05),而肾组织IL-10mRNA表达水平则升高(P<0.05)。结论肾康注射液可能通过抑制炎症反应对大鼠SAP肾损伤起治疗作用。Objective To observe the therapeutic effects of Shenkang injection on renal injury caused by severe acute pancreatitis (SAP) in rats .Methods Ninety male SD rats were randomly and equally divided into three group .Group A was taken as blank control .The rat model with SAP‐induced renal injury was constructed in groups of B and C .The rats in group B were intraperitoneally injected Shenkang injection 9 ml/kg at 3 hours after model establishment ,which was repeated every 12 hours . The rats in group C were intraperitoneally injected normal saline as model controls .Ten rats from each group were killed at 3 ,12 and 24 hours after injection for the measurements of serum levels of amylase ,creatinine and urea nitrogen (BUN ) .The tissue samples of the pancreas and kidney were taken for pathological observation and detections of NF‐κB p65 ,TNF‐αand IL‐6 mRNA expressions at the same time points .Results Compared with group C ,serum levels of amylase creatinine and BUN , the histopathology scores of rat pancreas and kidney ,and the expressions of NF‐κB p65 ,TNF‐α and IL‐6 mRNA of the kidney tissues were significantly decreased(P〈0 .05) ,but the expressions of IL‐10 mRNA were increased at 12 and 24 hours in group B(P〈0 .05) .Conclusion Shenkang injection has a therapeutic effect on SAP‐induced renal injury in rats by inhibiting inflammatory responses .
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