文章摘要
朱辰蕾,惠宇坚,张翔海,吴东迎,范卫民,胡 军.烟碱对膝骨关节炎模型大鼠的保护作用及机制研究[J].南京医科大学学报,2014,(2):129~134
烟碱对膝骨关节炎模型大鼠的保护作用及机制研究
Chondroprotective effects and mechanisms of nicotine on osteoarthritis in rat models
投稿时间:2013-05-13  
DOI:10.7655/NYDXBNS20140201
中文关键词: 骨关节炎  大鼠  烟碱  烟碱乙酰胆碱受体
英文关键词: osteoarthritis  rat  nicotine  nicotinic acetylcholine receptor
基金项目:国家自然科学基金(30901800)
作者单位
朱辰蕾 南京医科大学第一附属医院骨科,江苏 南京 210029
苏州大学附属第三医院骨科,江苏 常州 213000 
惠宇坚 南京医科大学第一附属医院骨科,江苏 南京 210029 
张翔海 马鞍山市人民医院骨科,安徽 马鞍山 243000 
吴东迎 南京医科大学第一附属医院骨科,江苏 南京 210029 
范卫民 南京医科大学第一附属医院骨科,江苏 南京 210029 
胡 军 南京医科大学第一附属医院骨科,江苏 南京 210029 
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中文摘要:
      目的:研究烟碱对碘乙酸(monoiodoacetic acid,MIA)诱导的大鼠膝骨关节炎模型的保护作用,并对其作用机制作初步探讨?方法:通过MIA膝关节腔注射法构建大鼠膝骨关节炎模型,将造模成功的30只SD大鼠随机分为模型组(MIA组)10只,烟碱干预组20只(MIA+Nic 0.25 mg/kg与MIA+Nic 0.5 mg/kg组各10只)?另外,将10只大鼠作为假手术组(对照组)?造模30 d后提取大鼠右膝关节软骨组织标本,进行大体光镜和组织学病理切片观察关节软骨破坏情况;并用RT-PCR法对各组大鼠右膝关节软骨内的Ⅱ型胶原?蛋白聚糖的表达进行检测;采用Western blot法检测磷酸化Akt蛋白表达?结果:与MIA组相比,烟碱可明显改善模型大鼠膝关节大体光镜评分和Mankin’s评分(P < 0.01),提高关节软骨Ⅱ型胶原和蛋白聚糖表达水平(P < 0.01),并显著增加磷酸化Akt蛋白水平(P < 0.01)?结论:烟碱可有效缓解MIA诱导的大鼠膝关节软骨退变,这种保护作用可能与PI3K/Akt信号途径有关?
英文摘要:
      Objective:To study the protective effects of nicotine on cartilage of monoiodoacetic acid(MIA)-induced rat osteoarthritis model. Methods:A total of 40 rats were randomly divided into four groups(control group,MIA group,MIA+Nic 0.25 mg/kg group and MIA+Nic 0.5 mg/kg group). Each group rats were sacrificed on 30th day after they received the first intra-articular injection of MIA(1mg) surgery. The right knee samples were carefully dissected. Generally light microscope and histological pathological examination were used to observe the destruction of articular cartilage. Reverse-transcription PCR was used to detect the gene expression of type II collagen and aggrecan. The protein expression of phosphor-Akt was measured by Western blot test. Results:Compared with the MIA group,nicotine treatment significantly decreased the light microscopy score and the Mankin’s score(P < 0.01) of the knee samples,and significantly increased the mRNA levels of typeⅡ collagen and aggrecan (P < 0.01) and the protein levels of phosphor-Akt (P < 0.01). Conclusion:Nicotine attenuates the severity of cartilage degeneration in the experimental rat model. These protective effects may partially benefit from the increase of phosphor-Akt expression.
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