[目的]观察盲肠结扎穿孔(Cecal ligation and puncture,CLP)所致的脓毒症诱导急性肾损伤(AKI)后大鼠不同时间点的血清及肾组织中NLRP3/ASC/caspase-1/IL-1β/IL-18的表达情况。[方法]建立大鼠CLP诱导的脓毒症AKI模型,并于手术后不同时...[目的]观察盲肠结扎穿孔(Cecal ligation and puncture,CLP)所致的脓毒症诱导急性肾损伤(AKI)后大鼠不同时间点的血清及肾组织中NLRP3/ASC/caspase-1/IL-1β/IL-18的表达情况。[方法]建立大鼠CLP诱导的脓毒症AKI模型,并于手术后不同时间点用ELISA试剂盒方法测定血清尿素氮(BUN)、血清肌酐(Scr)水平及IL-1β/IL-18的表达量;采用Western blotting法检测肾脏组织NLRP3/ASC/caspase-1/IL-1β/IL-18蛋白水平,并对肾脏组织进行HE染色病理分析。[结果]CLP诱导的脓毒症大鼠血清BUN和Scr水平显著增高,肾小管坏死也显著增加,均于CLP术后24 h达到高峰,与假手术组大鼠相比差异显著(P<0.05或P<0.01);大鼠肾脏组织中NLRP3/ASC/caspase-1/IL-1β/IL-18及血清IL-1β/IL-18水平也随着损伤程度的加重表现出升高趋势,与假手术组相比差异均达到显著水平。[结论]大鼠脓毒症AKI后肾组织或血清中NLRP3/ASC/caspase-1/IL-1β/IL-18蛋白水平表达增加,表明NLRP3炎症小体的激活可能对脓毒症AKI及其病理改变有促进作用。展开更多
Objective:To observe changes in the molecular expression of the NLR Family Pyrin Domain Containing Protein 3(NLRP3)pathway in depressed rats after treatment with Xiaoyaosan,and identify the regulatory mechanism of thi...Objective:To observe changes in the molecular expression of the NLR Family Pyrin Domain Containing Protein 3(NLRP3)pathway in depressed rats after treatment with Xiaoyaosan,and identify the regulatory mechanism of this compound.Methods:Male SpragueeD awley rats were randomly divided into five groups with 12 rats in each group,including the control group,model group,Fluoxetine group,Xiaoyaosan group,and MCC950 group.A depression model was generated by chronic immobilization stress(induced by 3 h of restraint immobilization every day),and the drugs were administered at the same time in each group for 21 days.The effects of Xiaoyaosan on behavioral changes of depressed rats were observed through macroscopic characterization,body mass,open field experiments,and a sucrose preference test.The m RNA and protein expression of the NLRP3 signaling pathway was examined by fluorescence real-time quantitative PCR and Western blot assays.Results:The Xiaoyaosan group,Fluoxetine group,and MCC950 group rats showed improved depressive behavior and an increased weight of sucrose water consumption.The protein and mRNA expression levels of NLRP3,Caspase-1,and IL-1 b were also decreased in the Fluoxetine,Xiaoyaosan,and MCC950 groups.Conclusion:NLRP3,Caspase-1,and IL-1 b protein and mRNA expression levels were increased in the cortex of depressed rats,while Xiaoyaosan protected cortical tissue in these rats by decreasing NLRP3,Caspase-1,and IL-1 b protein and mRNA expression.展开更多
文摘Objective:To observe changes in the molecular expression of the NLR Family Pyrin Domain Containing Protein 3(NLRP3)pathway in depressed rats after treatment with Xiaoyaosan,and identify the regulatory mechanism of this compound.Methods:Male SpragueeD awley rats were randomly divided into five groups with 12 rats in each group,including the control group,model group,Fluoxetine group,Xiaoyaosan group,and MCC950 group.A depression model was generated by chronic immobilization stress(induced by 3 h of restraint immobilization every day),and the drugs were administered at the same time in each group for 21 days.The effects of Xiaoyaosan on behavioral changes of depressed rats were observed through macroscopic characterization,body mass,open field experiments,and a sucrose preference test.The m RNA and protein expression of the NLRP3 signaling pathway was examined by fluorescence real-time quantitative PCR and Western blot assays.Results:The Xiaoyaosan group,Fluoxetine group,and MCC950 group rats showed improved depressive behavior and an increased weight of sucrose water consumption.The protein and mRNA expression levels of NLRP3,Caspase-1,and IL-1 b were also decreased in the Fluoxetine,Xiaoyaosan,and MCC950 groups.Conclusion:NLRP3,Caspase-1,and IL-1 b protein and mRNA expression levels were increased in the cortex of depressed rats,while Xiaoyaosan protected cortical tissue in these rats by decreasing NLRP3,Caspase-1,and IL-1 b protein and mRNA expression.
