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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: The incidence of brain injury in preterm infants is very high and the prognosis is poor. It is currently believed that intrauterine infection and inflammatory reaction are important factors that lead to brain injury in preterm infants. In this study, animal models of intrauterine infection were established by intraperitoneal injection of lipopolysaccharide (LPS) in pregnant rats to investigate whether dexamethasone (Dex) has a protective effect on brain injury in premature infants. Methods: Pregnant mice of 18 days pregnant were randomly divided into saline control group, LPS group and Dex intervention group, respectively, intraperitoneal injection of drugs. The expression of tumor necrosis factor (TNF) in fetal rat brain was observed by immunohistochemistry and RT-PCR 4 h after injection. The levels of tumor necrosis factor (TNF) in fetal rat brain were measured by in situ end labeling Apoptosis changes. Results: Compared with LPS group, the levels of TNF-α protein and mRNA in fetal brain of Dex intervention group were significantly decreased (P <0.05), and were negatively correlated with the dosage of Dex. The apoptotic cells in Dex intervention group were significantly decreased compared with LPS group (P <0.01). CONCLUSION: Intrauterine injection of LPS can cause brain injury in fetal rats. Dexamethasone may have a protective effect on brain injury induced by intrauterine infection by inhibiting the expression of TNF-α in fetal brain and reducing brain cell apoptosis.