【摘要】 目的:探讨受体酪氨酸激酶抑制剂genistein对兔OA模型软骨细胞NO的表达及软骨组织形态的影响,并探讨其可能的作用机制。方法:参照Hulth法建立兔骨关节炎模型,予以genistein干预后,分别按照0.1 mg.kg-1、0.2 mg.kg-1、0.3 mg.kg-1、0.4 mg.kg-1、0.5 mg.kg-1的给药剂量进行分组,行手术侧关节腔内注射,通过测定各组亚硝酸盐含量检测关节腔内NO的表达水平,同时进行软骨组织形态学检查。结果:0.3 mg.kg-1、0.4 mg.kg-1、0.5 mg.kg-1浓度genistein干预组关节腔内NO的表达水平明显低于对照组,差异具有统计学意义(P<0.05);对软骨组织行H.E/SOFG染色显示,在造模后第4周、第8周与第12周时,genistein干预组与对照组相比,组织损伤均明显减轻,Mankin评分均明显下降,差异具有统计学意义(P<0.05)。结论:受体酪氨酸激酶抑制剂genistein在体内能减少骨关节炎软骨细胞NO的表达,对于延迟关节软骨在组织形态水平的退变是有效的,但是尚不能最终阻止软骨退变发生发展的进程。更多还原

【Abstract】 Objective:To investigate the effects of recePtor tyrosine kinase inhibitor genistein on the exPression of NO and ultra-microstructure of osteoarthritis cartilage and chondrocyte in OA rats,thus try to exPress the Probable mechanisms involved.Methods:According to Hulth method,we built rat OA model and the exPression levels of NO was detected by Griess method and the change of ultra-microstructure of cartilage was observed.Results:ComPared with control grouP,less levels of NO were detected after the intervention of genistein(0.3 mg·kg-1、0.4 mg·kg-1 and 0.5 mg·kg-1)(P<0.05).At 4、8 and 12 weeks after oPeration,cartilage sections made and stain with HE/SOFG stain showed less injury,and Mankin score were significantly decreased in intervention grouPs comPared with control grouP(P<0.05).Conclusion:Genistein can reduced the exPression of NO in-vivo.The results of Mankin score and HE/SOFG stain showed that genistein Partly delayed the observation of ultra-microstructure of cartilage exPlored the alleviation of the ultra-microstructure damage of cartilage after injury.更多还原