环氧化酶-2在新生大鼠缺氧缺血性脑损伤的表达及NS398抗凋亡作用  

Cyclooxygenase-2 expression in neonatal rat with hypoxic-ischemic brain damage and the anti-apoptotic effect of NS398

作　　者：张萍[1] 李冬[2] 徐立新[2] 曲云霞[2] 

机构地区：[1]鞍山市中心医院儿科,辽宁鞍山114001 [2]大连医科大学附属第二医院儿科,辽宁大连116027

出　　处：《中国小儿急救医学》2006年第5期448-450,共3页Chinese Pediatric Emergency Medicine

摘　　要：目的探讨环氧化酶-2(COX-2)在新生儿缺氧缺血性脑损伤(HIBD)中的作用及其抑制剂NS398抗凋亡作用。方法新生大鼠HIBD模型为研究对象,半定量RT-PCR检测脑组织COX-2mRNA,免疫组化方法测定COX-2蛋白表达,光镜下观察神经元坏死情况,TUNEL法测定NS398抗凋亡作用。结果HIBD后COX-2表达出现不同程度的增强,在HIBD24h达高峰,同其余各组表达量相比均有显著性差异(P<0.01)。缺氧前、后加入NS398,脑组织神经元凋亡程度有不同程度的降低,与对照组比较有显著性差异(P<0.01),缺氧前给药组神经元凋亡程度低于缺氧后给药组(P<0.01)。结论COX-2在新生儿HIBD形成中发挥重要的作用。NS398具有一定的抗凋亡作用,且早期给予COX-2特异性抑制剂NS398可能更好地发挥其抗凋亡作用。Objective To investigate the effect of COX-2 on the pathogenesis of neonatal HIBD and the effect of NS398 on apoptosis. Methods Neonatal HIBD rat model was established. The brain tissues were collected for microscopic examinantion. The expression of COX-2 mRNA was measured by semi-quantitative RT-PCR, the expression of COX-2 protein was measured by immunohistochemiscal method, the anti-apoptotic effect to sis function of NS398 was estimated by TUNEL. Results The expression of COX-2 was significantly higher than that in control group, peaked at 24 h after hypoxia and ischemia. The neuron apoptosis in 24 h HIBD group was higher significlantly than that in treatment group（NS398）, P 〈 0.01. The apoptosis level in the group treated with antagonist NS398 1h before hypoxia was lower than that in the group treated with antagonist NS398 1h after hypoxia, （P 〈 0.01）. Conclusion COX-2 plays an important role in the pathogenesis of neonatal HIBD and COX-2 inhibitor has anti-apoptotic effect, which is more effective through early-stage intervention.

关 键 词：脑缺氧缺血 环氧化酶-2 NS398 

分 类 号：R722.12[医药卫生—儿科]