CAJ | 학술논문

目的建立膝关节骨性关节炎兔模型,观察其软骨和关节液中白细胞介素(IL)-1和IL-6的变化,探讨膝关节骨性关节炎发生发展的过程和发病机制.方法将30只成年新西兰大白兔(60个膝关节)随机分为2组,实验组(20只,40个膝关节)和对照组(10只,20个膝关节).通过内侧副韧带切断术和内侧半月板切除术建立骨性关节炎模型,实验组分别在术后第1、2、3、4周处死兔并取材.对照组在第4周处死兔并取材.采用墨汁染色法观察软骨损伤,使用光镜和扫描电镜观察膝关节软骨组织学的动态变化;采用酶联免疫吸附试验(ELISA)法测定膝关节液中IL-1和IL-6的表达.结果 (1)对照组股骨内髁Ⅰ级17例,Ⅱ级3例.实验组第1周股骨内髁Ⅱ级7例,Ⅲ级3例;2周Ⅱ级2例,Ⅲ级6例,Ⅳ级2例;3周Ⅲ级6例,Ⅳ级4例;4周Ⅱ级5例,Ⅳ级5例.(2)膝关节骨性关节炎模型兔关节软骨损伤随时间延长而加重,光镜和电镜的检查结果均显示关节软骨随时间延长而逐渐被破坏.(3)对照组IL-1和IL-6浓度分别为(22.37±1.46)和(119.25 ±9.94) ng/L,第1周时为(59.25±3.18)和(731.68±20.72) ng/L,第2周为(81.47±1.66)和(568.10±21.69) ng/L,第3周为(68.44±2.53)和(755.76±16.37) ng/L,第4周为(53.02±2.59)和(438.94±23.88) ng/L.关节液中IL-1和IL-6的表达明显升高,IL-1表达在2周时达到峰值,IL-6在第1周时即明显升高,第4周时下降,但仍处于较高水平.结论在兔膝关节骨性关节炎模型中,随着时间延长,兔模型的膝关节软骨损伤进行性加重,关节液中IL-1和IL-6水平呈高表达.
목적 건립슬관절골성관절염토모형,관찰기연골화관절액중백세포개소(IL)-1화IL-6적변화,탐토슬관절골성관절염발생발전적과정화발병궤제.방법 장30지성년신서란대백토(60개슬관절)수궤분위2조,실험조(20지,40개슬관절)화대조조(10지,20개슬관절).통과내측부인대절단술화내측반월판절제술건립골성관절염모형,실험조분별재술후제1、2、3、4주처사토병취재.대조조재제4주처사토병취재.채용묵즙염색법관찰연골손상,사용광경화소묘전경관찰슬관절연골조직학적동태변화;채용매련면역흡부시험(ELISA)법측정슬관절액중IL-1화IL-6적표체.결과 (1)대조조고골내과Ⅰ급17례,Ⅱ급3례.실험조제1주고골내과Ⅱ급7례,Ⅲ급3례;2주Ⅱ급2례,Ⅲ급6례,Ⅳ급2례;3주Ⅲ급6례,Ⅳ급4례;4주Ⅱ급5례,Ⅳ급5례.(2)슬관절골성관절염모형토관절연골손상수시간연장이가중,광경화전경적검사결과균현시관절연골수시간연장이축점피파배.(3)대조조IL-1화IL-6농도분별위(22.37±1.46)화(119.25 ±9.94) ng/L,제1주시위(59.25±3.18)화(731.68±20.72) ng/L,제2주위(81.47±1.66)화(568.10±21.69) ng/L,제3주위(68.44±2.53)화(755.76±16.37) ng/L,제4주위(53.02±2.59)화(438.94±23.88) ng/L.관절액중IL-1화IL-6적표체명현승고,IL-1표체재2주시체도봉치,IL-6재제1주시즉명현승고,제4주시하강,단잉처우교고수평.결론 재토슬관절골성관절염모형중,수착시간연장,토모형적슬관절연골손상진행성가중,관절액중IL-1화IL-6수평정고표체.
Objective To establish rabbiknee joinosteoarthritimodel, observe the changeof interleukin (IL)-1 and IL-6 in the cartilage and synovial fluid, and explore the developmenprocesand the pathogenesiof knee joinosteoarthritis.MethodThirty adulNew Zealand white rabbit(60 knees) were randomly divided into 2 groups: experimental group (20 cases, 40 knees) and control group (10 cases, 20 knees).The osteoarthritimodel waestablished by the medial collateral ligamenand medial meniscuresection.The rabbitwere sacrificed afirst, 2nd, 3rd and 4th week afteoperation.In the control group, the rabbitwere sacrificed afourth week.Using the ink staining the cartilage injury waobserved, and lighmicroscope and scanning electron microscope were applied to observe the dynamichangeof knee articulacartilage histologically.Enzyme linked immunosorbenassay (ELISA) waused to determine the expression of IL-1 and IL-6 in synovial fluid of the knee.ResultThe articulacartilage injury in the rabbiknee joinosteoarthritiinflammation model waaggravated with the extension of time.Lighmicroscopiand electron microscopiexaminationrevealed thathe articulacartilage wagradually destroyed ovetime.The concentrationof IL-1 and IL-6 in control group were (22.37 ± 1.46) and (119.25 ± 9.94) ng/L respectively, and those in experimental group afirst, 2nd, 3rd and 4th week were (59.25 ±3.18) and (731.68 ±20.72) ng/L, (81.47 ± 1.66) and (568.10 ±21.69) ng/L, (68.44 ± 2.53) and (755.76 ± 16.37) ng/L, and (53.02 ± 2.59) and (438.94 ± 23.88) ng/L, respectively.The expression of IL-1 and IL-6 in synovial fluid waincreased significantly.The expression of IL-1 a2nd week reached the peak.IL-6 waincreased markedly athe 1 sweek, and declined a4th week, bumaintained ahigh level.Conclusion In the rabbimodel of knee joinosteoarthritis, the knee joincartilage damage waaggravated with the extension of time, and IL-1 and IL-6 in the synovial fluid were highly expressed.