摘要
目的:早产儿脑损伤有很高的发病率且愈后很差,目前认为宫内感染、炎症反应是导致早产儿脑损伤的重要因素。本研究通过给予孕鼠腹腔注射脂多糖(LPS)制作宫内感染的动物模型,探讨地塞米松(Dex)对早产儿脑损伤是否具有保护作用。方法:将孕18d孕鼠随机分为盐水对照组、LPS组和Dex干预组,分别腹腔注射药物。采用免疫组化法及RT-PCR法观察腹腔注药4h后胎鼠脑肿瘤坏死因子(TNF)表达的变化;采用原位末端标记法检测注药48h后LPS组、对照组及干预组胎脑细胞凋亡的变化。结果:Dex干预组胎脑TNF-α蛋白水平及mRNA表达较LPS组明显减弱(P<0.05),且与Dex的剂量呈负相关。Dex干预组凋亡细胞与LPS组相比较明显减少(P<0.01)。结论:宫内注射LPS可导致胎鼠脑损伤,地塞米松可能通过抑制胎脑TNF-α的表达,降低脑细胞凋亡,对宫内感染致脑损伤具有保护作用。
Objective：Brain damage in the preterm infant has the high incidence and bad prognosis. It was regarded that intrauterine infection （IUI） and the response to inflammatory played important roles in the brain damage. The present study used intraperitoneal injection of lipopolysaccharide （LPS） to produce IUI rat model. Then the effect of dexamethasone （Dex） on fetal brain injury was investigated. Methods：Pregnant rats at gestation day 18 were randomly divided into three groups：saline control group （group A）,LPS group （group B） and Dex-treated group （group C）. Expression of tumor necrosis factor-α （TNF-α ） in fetal brain was measured by immunohistochemistry and RT-PCR 4 h after drug injection. Apototic cells in fetal brain were detected by TUNEL method 48 h after drug injection. Results：The expression of TNF-α protein and mRNA significantly decreased in Dex-treated group compared with that of LPS group （P〈0.05）. The dose of Dex and the expression level of TNF-α showed a negative correlation. The number of apoptotic cells in the fetal brain of Dex-treated group was significant lower than that of LPS group （P〈0.01）. Conclusion：Intrauterine injection of LPS caused fetal brain damage. Dex may play a protective role on brain damage through inhibiting the expression of TNF-α and reducing apoptosis cells in the barin.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2010年第2期197-200,共4页
Chinese Journal of Neuroanatomy
关键词
地塞米松
宫内感染
肿瘤坏死因子-Α
凋亡
dexamethasone
intrauterine infection
tumor necrosis factor-α
apoptosis
作者简介
通讯作者：王欣煜 电话：010-62558150—8400，E-mail：sjcwxy1225@sina．com
