淫羊藿苷抑制钛颗粒诱导的炎症反应  

Icariin inhibits titanium particle-induced inflammatory reaction

作　　者：崔京福 徐耀增[1] 朱世军[1] 朱锋[1] 付稳[1] 邵洪国[1] 耿德春[1] 

机构地区：[1]苏州大学附属第一医院骨科,江苏省苏州市215006

出　　处：《中国组织工程研究》2014年第16期2563-2569,共7页Chinese Journal of Tissue Engineering Research

基　　金：江苏省临床医学科技专项资助项目(BL2012004);国家自然科学基金资助项目(81101399;81272018;81372018);江苏省自然科学基金资助项目(BK2011303);江苏省研究生培养创新工程资助项目(CXZZ13_0835)~~

摘　　要：背景:体外实验表明,淫羊藿苷可抑制脂多糖诱导的急性肺炎,其抗炎作用在磨损颗粒存在的条件下是否依然有效?目的:通过体内外实验相结合的方法探讨淫羊藿苷对磨损颗粒诱导炎症反应的调控作用。方法:①体内实验:将80只雄性C57BL/6小鼠随机分为4组,钛组和钛+淫羊藿苷组采用钛诱导小鼠颅骨无菌炎症模型,对照组、淫羊藿苷组也进行相同手术过程,但不植入钛,淫羊藿苷组、钛+淫羊藿苷组建模当天灌胃给予淫羊藿苷200 mg/(kg·d),对照组、钛组灌胃给予等量的安慰剂,2周后酶联免疫吸附实验、定量RT-PCR检测肿瘤坏死因子α,白细胞介素1β蛋白或mRNA的表达量。②体外实验:将小鼠单核/巨噬细胞RAW264.7分别与核因子кB受体配体、核因子кB受体配体+淫羊藿苷、核因子кB受体配体+钛颗粒及核因子кB受体配体+钛颗粒+淫羊藿苷共培养72 h,ELISA检测培养基上清中肿瘤坏死因子α,白细胞介素1β水平,RT-PCR分析肿瘤坏死因子α,白细胞介素1β基因mRNA表达。结果与结论:①体内实验:在钛颗粒存在的条件下,口服淫羊藿苷可明显减少颗粒诱导的炎症细胞浸润,使炎性增厚的骨膜变薄,抑制颅骨标本中肿瘤坏死因子α,白细胞介素1β的表达。②体外实验:经钛颗粒刺激后,细胞培养基中肿瘤坏死因子α,白细胞介素1β质量浓度显著增加,细胞中相应mRNA表达量上调,而经淫羊藿苷干预后这两种炎性因子在蛋白和基因水平的表达量显著下调。结果表明淫羊藿苷在体内外均可显著抑制钛颗粒诱导的炎症反应。BACKGROUND：Studiesin vitro have suggested that icarin can attenuate lipopolysaccharide （LPS）-induced acute pneumonia. Is the anti-inflammatory effect of icarin stil valid in the presence of wear particles？ OBJECTIVE：With studiesin vivo andin vitro, to investigate the regulatory effect of icarrin on titanium particle-induced inflammatory reaction. METHODS：（1） Studiesin vivo： Eighty male C57BL/6 mice aged 6-8 weeks were randomly divided into four groups： control group, icarin group, titanium particle group, and titanium particle＋icarin group. Mice in the titanium particle group and titanium particle＋icarin group received surgical procedure, and sterile and endotoxin-free titanium particles were implanted on the calvaria surfaces to induce inflammatory reaction. Mice in the control group and icarin group received the same surgery, but no wear particles were implanted. Then icarin was given oraly to mice in the titanium particle group and titanium particle＋ icarin group with a dose of 200 mg/kg per day for 2 weeks from the day of modeling. Mice in the control group and icarin group were given oraly the same dose of placebo. Two weeks later, tumor necrosis factor-α and interleukin-1β at protein and mRNA levels were respectively detected with enzyme-linked immunohistochemical （ELISA） and quantitative real time reverse transcription PCR （qRT-PCR） analysis. （2） Studiesin vitro： Mouse monocyte/macrophage RAW264.7 cels were cultured with different conditioned media： control group, nuclear factor receptor ligand кB （RANKL）; icarin group, RANKL＋icarin; titanium particle group, RANKL＋titanium particles; titanium particle＋icarrin group, RANKL＋icarin＋titanium particles. Titanium particles stimulated RAW264.7 cels were co-cultured with RANKL and icarin for 72 hours. Tumor necrosis factor-α and interleukin-1β at protein and mRNA levels in the supernatant were detected with ELISA analysis and qRT-PCR, respectively. RESULTS AND CONCLUSION： （1） Resultsin vivo： icar

关 键 词：生物材料 材料相容性 淫羊藿苷 钛颗粒 炎症反应 肿瘤坏死因子Α 白细胞介素1Β 国家自然科学基金 

分 类 号：R318[医药卫生—生物医学工程]