新生大鼠窒息后肾组织Omi/HtrA2表达及Ucf-101干预效果  

Effects of Ucf-101 on expression of Omi/HtrA2 in kidneys of postasphyxial neonatal rats

作　　者：花兵[1] 董文斌[1] 李清平[1] 冯志强[2] 余鸿[3] 翟雪松[1] 雷小平[1] 

机构地区：[1]四川泸州医学院附属医院新生儿科 [2]四川泸州医学院生理学教研室,四川泸州646000 [3]四川泸州医学院组织胚胎学教研室,四川泸州646000

出　　处：《中国当代儿科杂志》2010年第8期658-661,共4页Chinese Journal of Contemporary Pediatrics

基　　金：四川省杰出青年学科带头人培养基金(编号:04ZQ026-033);四川省科技厅应用基础项目(编号:2008JY0015);中华儿科杂志第一届双鹤珂立苏科研基金

摘　　要：目的探讨Omi/HtrA2在新生鼠窒息后肾组织的变化及Ucf-101的干预作用。方法将72只7～10dWistar大鼠随机分为对照组、窒息组和Ucf-101组。窒息组和Ucf-101组大鼠制成常压窒息模型。在窒息30min后复氧2、24、48h时采用免疫组化法检测各组肾组织中Omi/HtrA2的表达。采用TUNEL法检测肾凋亡细胞的形态及数量变化。结果窒息复氧后2hOmi/HtrA2表达开始增强,于24h达最高峰,随后有所下降。与窒息组相比,Ucf-101组各个时相点Omi/HtrA2的表达阳性率明显降低(P<0.01)。窒息复氧后2h,肾组织开始出现肾小管上皮细胞凋亡,24h凋亡细胞数达到高峰,而Ucf-101组各个时相点凋亡指数较窒息组均有明显减少。结论新生大鼠窒息后肾组织Omi/HtrA2表达增强,参与肾损伤;Ucf-101可使Omi/HtrA2的表达下降,从而抑制肾小管上皮细胞凋亡。Objective To investigate the expression of serine protease Omi/HtrA2 in kidneys of postasphyxial neonatal rats,and to study the effects of Ucf-101 on apoptosis and the expression of Omi/HtrA2 in these rats.Methods Seventy-two neonatal Wistar rats of 7-10 days old were randomly divided into 3 groups：control,postasphyxial model,Ucf-101-treated postasphyxial.The postasphyxial model was established by normobaric asphyxia.Expression of Omi/HtrA2 was determined with streptavidin-peroxidase immunohistochemistry 2,24 and 48 hrs after asphyxia.Terminal deoxynuleotidyl-mediated nick end labeling（TUNEL）was used to ascertain the apoptosis of renal cells.Results Compared with the control group,Omi/HtrA2 expression in renal cells began to increase 2 hrs after asphyxia and peaked at 24 hrs.The expression of Omi/HtrA2 in the Ucf-101-treated postasphyxial group was significantly lower than that in the postasphyxial model group（P〈0.01）.TUNEL-positive cells began to increase 2 hrs after asphyxia and peaked at 24 hrs in the postasphyxial model group when compared with the control group.The number of TUNEL-positive cells in the Ucf-101-treated postasphyxial group was significantly lower than that in the postasphyxial model group at all time points（P〈0.01）.Conclusions The expression of Omi/HtrA2 in kidneys is increased in postasphyxial neonatal rats.The increased Omi/HtrA2 expression may play an important role in the development of postasphyxial renal injury.Treatment with Ucf-101 can reduce the expression of Omi/HtrA2 in kidneys of postasphyxial neonatal rats and thus reduce renal tububar epithelial cell apoptosis.

关 键 词：窒息 肾损伤 OMI/HTRA2 Ucf-101 细胞凋亡 新生大鼠 

分 类 号：R722.12[医药卫生—儿科]