多聚鸟苷酸干预大鼠矽肺纤维化的内质网应激作用机制
发布时间：2018-11-17 11:42
【摘要】：目的探讨肌醇需求激酶1(IRE1)介导的内质网应激(ERS)细胞凋亡途径在多聚鸟苷酸(PolyG)干预大鼠矽肺纤维化中的作用及机制。方法将无特定病原体级成年雄性SD大鼠随机分为对照组(24只)、矽肺模型组(24只)、PolyG预防组(16只)和PolyG治疗组(16只),采用一次性吸入式气管滴注法,对照组大鼠予灭菌0.9%氯化钠溶液1 mL,其余3组大鼠均予质量浓度为50.0 g/L的矽尘混悬液1 mL以构建矽肺纤维化大鼠模型。PolyG预防组大鼠于造模当天,PolyG治疗组大鼠于造模第28天,均一次性经尾静脉注射剂量为2.5 mg/kg体质量的PolyG,于PolyG给药后第28和56天各处死大鼠8只。观察各组大鼠肺组织病理改变情况,以免疫印迹法测定葡萄糖调节蛋白-78(GRP78)、IRE1、CCAAT/增强子结合蛋白同源蛋白(CHOP)、半胱氨酸天冬氨酸蛋白酶(Casepase)-3、Casepase-12、Ⅰ型胶原和Ⅲ型胶原的蛋白相对表达水平。结果病理组织学检查结果显示:对照组大鼠肺组织结构正常;矽肺模型组大鼠肺组织肺泡结构破坏严重,出现纤维细胞性结节及大量胶原沉积;PolyG预防组和PolyG治疗组大鼠矽结节及胶原沉积均较矽肺模型组减少。矽肺模型组大鼠肺组织中GRP78、IRE1、CHOP、Caspase-3、Caspase-12、Ⅰ型胶原和Ⅲ型胶原的蛋白相对表达水平均高于对照组(P0.05)。除PolyG预防组IRE1和CHOP外,PolyG预防组和治疗组大鼠上述7个蛋白指标的表达水平均低于矽肺模型组(P0.05),但仍高于对照组(P0.05)。造模后第56天,PolyG预防组GRP78、IRE1、Caspase-3、Caspase-12、Ⅰ型胶原和Ⅲ型胶原的蛋白相对表达水平均低于PolyG治疗组(P0.05)。结论 IRE1介导的ERS未折叠蛋白反应可能参与了PolyG干预大鼠矽肺纤维化的过程;PolyG可有效预防和治疗矽肺纤维化,以预防性给药效果更佳。
[Abstract]:Objective to investigate the role and mechanism of inositol demand kinase 1 (IRE1) -mediated endoplasmic reticulum stress (ER) induced apoptosis of (ERS) cells in rats with silicosis induced by polyguanosine monophosphate (PolyG). Methods Adult male SD rats were randomly divided into control group (n = 24), silicosis model group (n = 24) and PolyG treatment group (n = 16). Rats in the control group were given sterilizing 0.9% sodium chloride solution 1 mL, and the other three groups were given silica dust suspension of 50.0 g / L for 1 mL to establish silicosis fibrosis model. The rats in the PolyG prevention group were treated with the model on the same day. On the 28th day of model making, 8 rats in PolyG group were killed on the 28th and 56th day after administration of PolyG with PolyG, of 2.5 mg/kg body mass injected via caudal vein. The pathological changes of lung tissue in each group were observed. Glucose regulated protein-78 (GRP78), IRE1,CCAAT/ enhancer binding protein homologous protein (CHOP), caspase (Casepase) 3 and casepase-12 were determined by Western blot. The relative expression level of type I collagen and type 鈪，
本文编号：2337660
[Abstract]:Objective to investigate the role and mechanism of inositol demand kinase 1 (IRE1) -mediated endoplasmic reticulum stress (ER) induced apoptosis of (ERS) cells in rats with silicosis induced by polyguanosine monophosphate (PolyG). Methods Adult male SD rats were randomly divided into control group (n = 24), silicosis model group (n = 24) and PolyG treatment group (n = 16). Rats in the control group were given sterilizing 0.9% sodium chloride solution 1 mL, and the other three groups were given silica dust suspension of 50.0 g / L for 1 mL to establish silicosis fibrosis model. The rats in the PolyG prevention group were treated with the model on the same day. On the 28th day of model making, 8 rats in PolyG group were killed on the 28th and 56th day after administration of PolyG with PolyG, of 2.5 mg/kg body mass injected via caudal vein. The pathological changes of lung tissue in each group were observed. Glucose regulated protein-78 (GRP78), IRE1,CCAAT/ enhancer binding protein homologous protein (CHOP), caspase (Casepase) 3 and casepase-12 were determined by Western blot. The relative expression level of type I collagen and type 鈪，
本文编号：2337660
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