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目的观察产前使用地塞米松(dexamethasone,DEX)对新生大鼠坏死性小肠结肠炎(necrotizing enterocoli-tis,NEC)发生率及肠道Toll样受体4(toll like receptor 4,TLR4)表达的影响,探讨其对NEC的保护作用及可能的机制。方法实验分为正常对照组、产前地塞米松干预组(DEX组)、产前生理盐水干预组(normal saline,NS组)3组,于孕16、17、18 d时DEX组孕鼠肌肉注射DEX 0.5 mg/(kg.d),NS组每天注射NS 0.3 ml。DEX组及NS组所生新生鼠建立NEC动物模型。正常对照组不予处理。于第5天处死新生鼠,观察近回盲部肠组织病理变化并做评分;免疫组化法检测TLR4蛋白的表达;其余小肠部分Q-PCR法检测TLR4 mRNA的表达。结果与NS组相比,DEX组新生鼠NEC发生率明显降低(P<0.01)。正常对照组未出现NEC症状,NS组新生鼠出现典型的NEC症状,DEX组NEC症状比NS组出现得更晚、更轻;与正常对照组相比,DEX组和NS组肠组织病理学评分及TLR4表达显著增高(P<0.05);与NS组相比,DEX组肠组织病理学评分及TLR4表达显著降低(P<0.05)。结论产前使用DEX对NEC大鼠具有保护作用,其机制可能是通过降低TLR4的表达从而发挥抗炎效应。
Objective To observe the incidence of necrotizing enterocoli-tis (NEC) and the expression of toll like receptor 4 (TLR4) in neonatal rats after prenatal dexamethasone (DEX) Influence, discuss its protective effect to NEC and possible mechanism. Methods The experiment was divided into three groups: normal control group, pre-dexamethasone intervention group (DEX group), prenatal saline group (NS group). At the 16th, 17th and 18th day of gestation, Injection of DEX 0.5 mg / (kg.d), NS group daily injection of NS 0.3 ml. NEC animal models were established in neonatal rats born in DEX group and NS group. Normal control group did not deal with. Neonatal rats were killed on the 5th day, pathological changes of ileum near the ileocecal part were observed and evaluated. The expression of TLR4 protein was detected by immunohistochemistry. The expression of TLR4 mRNA was detected by Q-PCR in the other small intestine. Results Compared with NS group, the incidence of NEC in DEX group was significantly decreased (P <0.01). NEC symptoms did not appear in the normal control group, typical symptoms of NEC in NS group, NEC symptom in DEX group appeared later and lighter than NS group. Compared with normal control group, the histopathological score (P <0.05). Compared with NS group, the histopathological score and TLR4 expression in DEX group were significantly decreased (P <0.05). Conclusion Prenatal use of DEX has a protective effect on NEC rats. The mechanism may be through anti-inflammatory effects by reducing the expression of TLR4.