摘要
目的探讨抗炎药地塞米松延缓下颌骨缺损骨再生的相关分子机制。方法建立SD大鼠双侧下颌骨颊舌向贯穿的骨缺损模型,随机分为用药组与生理盐水对照组,分别给予治疗剂量的地塞米松或者等体积的生理盐水,连续给药5 d后的第1、3、6、10、17天分别处死大鼠并取双侧下颌骨,用免疫组化染色,分别检测骨再生修复不同阶段炎症因子环氧化酶-2(COX2)、成骨分化关键性调控因子runt相关转录因子-2(RUNX2)及骨钙蛋白(BGP)的表达。结果炎症因子COX2及成骨因子RUNX2、BGP在骨再生修复过程中的表达存在相同的变化趋势,半定量数据表明RUNX2、BGP表达和COX2表达存在正相关关系。结论抗炎药地塞米松通过抑制炎症阶段COX2表达,从而抑制成骨分化关键性调控因子RUNX2/BGP表达,导致下颌骨缺损再生修复的延迟。
Objective To investigate the molecular mechanisms of dexamethasone delaying bone regeneration of mandible defect.Methods Bilateral mandibular bone defect model of SD rats were established.SD rats were divided into two groups randomly.The experiment group was administered with treatment of dose dexamethasone sodium phosphate,and the control group was administered with equal dose of physiologic saline.The rats were respectively killed on the first,third,sixth,tenth and seventeenth day after five days′ continuous administration,and the mandible samples were fixed,decacified,embedded,and sectioned.The expression of inflammatory factors cyclooxygenase-2(COX2)、osteogenic differentiation key regulatory factor runt-related transcription factor 2(RUNX2)and osteocalcin(BGP)during different stages of bone regenerationand was evaluated by immunohistochemistry.Results A similar expression trend between inflammatory factors COX2 and osteogenic factor RUNX2、BGP during bone regeneration was observed.Semi-quantitative data showed that there were positive relation among the expression of RUNX2、BGP and COX2.Conclusions Anti-inflammatory drug dexamethasone decreases the expression of osteogenic differentiation key regulatory molecules RUNX2/BGP by inhibiting the expression of COX2 during inflammatory phase,which delays bone regeneration of mandibular defect.
出处
《口腔医学》
CAS
2011年第4期206-209,共4页
Stomatology
基金
江苏省高校自然科学研究项目资助(09kjb320003)
