脂氧素A4及相关炎症因子在金黄地鼠口腔黏膜溃疡病灶中的表达  

Expression of Lipoxin A4 and Associated Inflammatory Factors in the Focus of Oral Mucosa Ulcer in the Golden Hamsters

作　　者：王学莹[1] 关为群[1] 宋典坤[2] 

机构地区：[1]福建医科大学附属协和医院口腔科,福建福州350001 [2]福建医科大学口腔医学院

出　　处：《口腔医学研究》2013年第8期699-703,共5页Journal of Oral Science Research

摘　　要：目的:研究脂氧素A4对口腔溃疡愈合的可能影响。方法:以"自由基损伤法"建立实验组金黄地鼠口腔黏膜溃疡模型,分别于建模后第3、6、10天处死A、B、C组动物。D组不做任何干预,第10天处死。切取病灶组织检测NF-κB p65表达强度及LXA4、PGE2浓度。结果:LXA4浓度和PGE2浓度在A、B、C组显著高于D组。LXA4浓度、PGE2浓度、NF-κB p65表达强度呈正相关。结论:口腔黏膜溃疡的"自限性"愈合可能与LXA4、PGE2抑制NF-κB所介导的炎症级联反应相关。Objective： To study the possible mechanism of LXA4 effecting on the healing of ulcer. Methods： Using ＂reactive oxygen species induction＂ method to set up the oral mucosa ulcer model of golden hamsters of the group A,B and C. Then we sacrificed the animals in groupA,B,C at the day after seting--up 3 days,6 days,10 days re- spectively . The animals in group D were kept without any intervention, and sacrificed the 10th day. The tissue were collected for the detection of nuclear factor-κB （NF-κB） p65 and the level of LXA4 and prostaglandin E2 （PGE2） Results： Both LXA4 and PGE2 levels in group A,B,C were significantly higher than those in group D. Each two of the level of LXA4 ,level of PGE2 and the staining of NF-κB p65 were positive correlation. Conclusion： The ＂self --limitation＂ of oral mucosa ulcer may associate with cascade reaction induced by LXA4,PGE2 and NF-κB.

关 键 词：脂氧素 口腔溃疡 核因子-ΚB 前列腺素 金黄地鼠 

分 类 号：R781.5[医药卫生—口腔医学]