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目的探讨高氧致新生大鼠肺组织损伤过程中晚期糖基化终末产物受体(RAGE)的表达情况。方法将16只3日龄新生大鼠依据是否高浓度氧暴露随机分为空气组(空气环境下暴露7天)大鼠和高氧组(95%氧暴露7天)大鼠,并进行比较观察。在此实验结束后,留取大鼠的肺组织标本和静脉血标本,通过光镜观察并盲法评分比较其肺组织辐射状肺泡计数(radic alalveolar counts,RAC)、RT-PCR法检测肺组织匀浆RAGEmRNA表达、免疫组化法检测肺组织RAGE的表达情况、ELASA法检测血清及肺泡灌洗液(BALF)TNF及sRAGE的水平。结果高氧组大鼠组肺组织损伤RAC降低(t=14.87,P=0.000)、肺组织RAGEmRNA增加(t=9.7109,P=0.000)、RAGE蛋白表达增加、BALFTNF-α(t=9.807,P=0.000)增高、sRAGE水平下降(t=3.7484,P=0.000)。结论 RAG通路在新生大鼠高氧引致肺组织损伤中具有重要的作用。
Objective To investigate the expression of advanced glycation end product receptor (RAGE) in the lung tissue of neonatal rats with hyperoxia-induced lung injury. Methods Twenty-six 3-day-old neonatal rats were randomly divided into two groups: air group (exposed to air for 7 days) and hyperoxia group (exposed to 95% oxygen for 7 days) . At the end of this experiment, rat lung tissue samples and venous blood samples were collected, radicle alalveolar counts (RAC) of lung tissue were observed by light microscopy, and lung tissue was detected by RT-PCR The expression of RAGEmRNA was detected by immunohistochemistry. The levels of TNF and sRAGE in serum and alveolar lavage fluid (BALF) were detected by ELASA. Results Compared with the control group, the level of RAC in lung tissue of rats in hyperoxia group decreased (t = 14.87, P = 0.000), RAGE mRNA increased (t = 9.7109, P = 0.000) = 0.000), sRAGE level decreased (t = 3.7484, P = 0.000). Conclusion RAG pathway plays an important role in lung injury caused by hyperoxia in neonatal rats.