中华风湿病学杂志
中華風濕病學雜誌
중화풍습병학잡지
CHINESE JOURNAL OF RHEUMATOLOGY
2011年
8期
550-552,后插1
,共4页
关节炎,类风湿%高迁移率族蛋白质类%雷公藤属%甲氨蝶呤
關節炎,類風濕%高遷移率族蛋白質類%雷公籐屬%甲氨蝶呤
관절염,류풍습%고천이솔족단백질류%뢰공등속%갑안접령
Arthritis,rheumatoid%High-mobility group proteins%Tripterygium%Methotrexate
目的 探讨高迁移率族蛋白B1(HMGB1)在类风湿关节炎(RA)治疗中的作用及雷公藤多苷治疗RA的可能机制.方法 建立胶原诱导性关节炎(CIA)大鼠模型建立后,将造模成功的大鼠随机分为模型组、甲氨蝶呤治疗组、雷公藤多苷治疗组、雷公藤多苷和甲氨蝶呤联合治疗组进行药物干预,4周后取材,采用免疫组织化学法检测HMGB1在正常组、模型组和各治疗组大鼠的滑膜与关节中的表达,采用酶联免疫吸附试验(ELISA)法检测HMGB1在正常组、模型组和各治疗组大鼠血清中的含量.统计方法采用方差分析.结果 HMGB1在模型组大鼠滑膜、关节中的蛋白表达以及血清中的含量[(23.8±2.2)ng/ml]明显高于正常组[(7.4±1.6)ng/ml](P＜0.01),3个治疗组大鼠滑膜、关节中HMGB1的表达和血清中HMGB1的含量[分别为(133±3.1),(17.4±4.9),(11.7±1.5)ng/ml]显著低于模型组(P＜0.01),但又高于正常组(P＜0.05).结论 HMGB1参与了CIA滑膜增生、软骨和骨质破坏的病理过程;甲氨蝶呤与雷公藤多苷治疗RA滑膜炎和骨质破坏的分子机制与其降低HMGB1的表达相关.
目的 探討高遷移率族蛋白B1(HMGB1)在類風濕關節炎(RA)治療中的作用及雷公籐多苷治療RA的可能機製.方法 建立膠原誘導性關節炎(CIA)大鼠模型建立後,將造模成功的大鼠隨機分為模型組、甲氨蝶呤治療組、雷公籐多苷治療組、雷公籐多苷和甲氨蝶呤聯閤治療組進行藥物榦預,4週後取材,採用免疫組織化學法檢測HMGB1在正常組、模型組和各治療組大鼠的滑膜與關節中的錶達,採用酶聯免疫吸附試驗(ELISA)法檢測HMGB1在正常組、模型組和各治療組大鼠血清中的含量.統計方法採用方差分析.結果 HMGB1在模型組大鼠滑膜、關節中的蛋白錶達以及血清中的含量[(23.8±2.2)ng/ml]明顯高于正常組[(7.4±1.6)ng/ml](P＜0.01),3箇治療組大鼠滑膜、關節中HMGB1的錶達和血清中HMGB1的含量[分彆為(133±3.1),(17.4±4.9),(11.7±1.5)ng/ml]顯著低于模型組(P＜0.01),但又高于正常組(P＜0.05).結論 HMGB1參與瞭CIA滑膜增生、軟骨和骨質破壞的病理過程;甲氨蝶呤與雷公籐多苷治療RA滑膜炎和骨質破壞的分子機製與其降低HMGB1的錶達相關.
목적 탐토고천이솔족단백B1(HMGB1)재류풍습관절염(RA)치료중적작용급뢰공등다감치료RA적가능궤제.방법 건립효원유도성관절염(CIA)대서모형건립후,장조모성공적대서수궤분위모형조、갑안접령치료조、뢰공등다감치료조、뢰공등다감화갑안접령연합치료조진행약물간예,4주후취재,채용면역조직화학법검측HMGB1재정상조、모형조화각치료조대서적활막여관절중적표체,채용매련면역흡부시험(ELISA)법검측HMGB1재정상조、모형조화각치료조대서혈청중적함량.통계방법채용방차분석.결과 HMGB1재모형조대서활막、관절중적단백표체이급혈청중적함량[(23.8±2.2)ng/ml]명현고우정상조[(7.4±1.6)ng/ml](P＜0.01),3개치료조대서활막、관절중HMGB1적표체화혈청중HMGB1적함량[분별위(133±3.1),(17.4±4.9),(11.7±1.5)ng/ml]현저저우모형조(P＜0.01),단우고우정상조(P＜0.05).결론 HMGB1삼여료CIA활막증생、연골화골질파배적병리과정;갑안접령여뢰공등다감치료RA활막염화골질파배적분자궤제여기강저HMGB1적표체상관.
Objective To investigate the role of high-mobility group box-1 (HMGB1) in the pathogenesis and the treatment of rheumatoid arthritis (RA) and the pathogenesis of TWP in treatment of RA.Methods A rat model of collagen induced arthritis (CIA) was developed and CIA rats were divided into the model group, the TWP group, the MTX group and the combination treatment group. And the tissues and blood were drawn from the rats 4 weeks later. HMGB1 expression in synovium, joint and the sera were tested by immunohistochemical stain and ELISA. Results HMGB l expression of the model in the synovium, joint and serum [(23.8±2.2) ng/ml] were remarkably higher than the control [(7.4±1.6) ng/ml] (P＜0.01); HMGB1 expression of the treatment groups in synovium, joint and serum [ (13.3±3.1), (17.4±4.9), (11.7±1.5 ) ng/ml]is obviously lower than the model (P＜0.01), and were higher than that of the controls(P＜0.05). Conclusion HMGB1 participates in the hyperplasia of synovial membrane, cartilage and bone destruction of CIA. The molecular mechanism for the TWP and MTX in the trentment of synovitis and bone destruction of RA is correlated with the expression of HMGB1.
