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

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7~10 d Wistar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30 min后复氧2、24、48 h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2 h Omi／HtrA2表达开始增强，于24 h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2 h，肾组织开始出现肾小管上皮细胞凋亡，24 h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。［中国当代儿科杂志，2010，12（8）：658-661］

Abstract:

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.［Chin J Contemp Pediatr, 2010, 12 (8):658-661］