中华风湿病学杂志
中華風濕病學雜誌
중화풍습병학잡지
CHINESE JOURNAL OF RHEUMATOLOGY
2009年
2期
123-126
,共4页
杜金烽%李芬%田静%谢希%陈进伟%高洁生
杜金烽%李芬%田靜%謝希%陳進偉%高潔生
두금봉%리분%전정%사희%진진위%고길생
白藜芦醇%关节炎,胶原诱导性
白藜蘆醇%關節炎,膠原誘導性
백려호순%관절염,효원유도성
Resveratrol%Arthritis,collagen induced
目的 观察白藜芦醇对胶原诱导大鼠关节炎(CIA)的抗炎作用.方法 选择牛Ⅱ型胶原(CⅡ)为免疫原,建立CIA模型.选取42只造模成功的大鼠随机分为7组:模型组;来氟米特(LEF)对照组;白芍总苷(TGP)对照组;甲氨蝶呤(MTX)对照组;白藜芦醇(Res)小剂量组;白藜芦醇中剂量组;白藜芦醇高剂量组.采用关节炎指数评分(AI)法对大鼠关节炎症程度进行评分;采用酶联免疫吸附试验(ELISA)方法测定各组大鼠血清中抗CⅡ抗体水平.结果 AI评分:低剂量白藜芦醇组与模型组比较差异无统计学意义(12.3±0.5与12.8±0.4);高剂量白藜芦醇组低于中、低剂量组(6.0±0.6与8.2±1.0,12.3±0.5,P<0.01).高剂量白藜芦醇组低于白芍总苷组(6.0±0.6与8.8±0.8,P<0.01);LEF组低于TGP组、MTX组、3组白藜芦醇组(4.7±0.5与8.9±0.8,6.4+0.5,P<0.01);血清抗CⅡ抗体水平:模型组明显高于LEF组、MTX组、TGP组及高、中剂量白藜芦醇组(0.928±0.021与0.391±0.016,0.503±0.010,0.525±0.015,0.507±0.01,0.570±0.021,P<0.01),而与低剂量白藜芦醇组之间差异无统计学意义(0.928±0.021与0.908±0.026);高剂量白藜芦醇组低于白芍总苷组及低剂量白藜芦醇组(0.507±0.01与0.525±0.015,0.908±0.026,P<0.01);LEF组低于高、中剂量白藜芦醇组(0.391±0.026与0.507±0.010,0.570±0.021,P<0.01).结论 ①高、中剂量白藜芦醇能够缓解CIA的炎症症状,而低剂量白藜芦醇则无此作用.②中等剂量白藜芦醇对CIA大鼠的短期疗效与TGP相当,高剂量白藜芦醇的疗效强于TGP,但弱于LEF.③白藜芦醇能够抑制血清抗CⅡ抗体的生成.
目的 觀察白藜蘆醇對膠原誘導大鼠關節炎(CIA)的抗炎作用.方法 選擇牛Ⅱ型膠原(CⅡ)為免疫原,建立CIA模型.選取42隻造模成功的大鼠隨機分為7組:模型組;來氟米特(LEF)對照組;白芍總苷(TGP)對照組;甲氨蝶呤(MTX)對照組;白藜蘆醇(Res)小劑量組;白藜蘆醇中劑量組;白藜蘆醇高劑量組.採用關節炎指數評分(AI)法對大鼠關節炎癥程度進行評分;採用酶聯免疫吸附試驗(ELISA)方法測定各組大鼠血清中抗CⅡ抗體水平.結果 AI評分:低劑量白藜蘆醇組與模型組比較差異無統計學意義(12.3±0.5與12.8±0.4);高劑量白藜蘆醇組低于中、低劑量組(6.0±0.6與8.2±1.0,12.3±0.5,P<0.01).高劑量白藜蘆醇組低于白芍總苷組(6.0±0.6與8.8±0.8,P<0.01);LEF組低于TGP組、MTX組、3組白藜蘆醇組(4.7±0.5與8.9±0.8,6.4+0.5,P<0.01);血清抗CⅡ抗體水平:模型組明顯高于LEF組、MTX組、TGP組及高、中劑量白藜蘆醇組(0.928±0.021與0.391±0.016,0.503±0.010,0.525±0.015,0.507±0.01,0.570±0.021,P<0.01),而與低劑量白藜蘆醇組之間差異無統計學意義(0.928±0.021與0.908±0.026);高劑量白藜蘆醇組低于白芍總苷組及低劑量白藜蘆醇組(0.507±0.01與0.525±0.015,0.908±0.026,P<0.01);LEF組低于高、中劑量白藜蘆醇組(0.391±0.026與0.507±0.010,0.570±0.021,P<0.01).結論 ①高、中劑量白藜蘆醇能夠緩解CIA的炎癥癥狀,而低劑量白藜蘆醇則無此作用.②中等劑量白藜蘆醇對CIA大鼠的短期療效與TGP相噹,高劑量白藜蘆醇的療效彊于TGP,但弱于LEF.③白藜蘆醇能夠抑製血清抗CⅡ抗體的生成.
목적 관찰백려호순대효원유도대서관절염(CIA)적항염작용.방법 선택우Ⅱ형효원(CⅡ)위면역원,건립CIA모형.선취42지조모성공적대서수궤분위7조:모형조;래불미특(LEF)대조조;백작총감(TGP)대조조;갑안접령(MTX)대조조;백려호순(Res)소제량조;백려호순중제량조;백려호순고제량조.채용관절염지수평분(AI)법대대서관절염증정도진행평분;채용매련면역흡부시험(ELISA)방법측정각조대서혈청중항CⅡ항체수평.결과 AI평분:저제량백려호순조여모형조비교차이무통계학의의(12.3±0.5여12.8±0.4);고제량백려호순조저우중、저제량조(6.0±0.6여8.2±1.0,12.3±0.5,P<0.01).고제량백려호순조저우백작총감조(6.0±0.6여8.8±0.8,P<0.01);LEF조저우TGP조、MTX조、3조백려호순조(4.7±0.5여8.9±0.8,6.4+0.5,P<0.01);혈청항CⅡ항체수평:모형조명현고우LEF조、MTX조、TGP조급고、중제량백려호순조(0.928±0.021여0.391±0.016,0.503±0.010,0.525±0.015,0.507±0.01,0.570±0.021,P<0.01),이여저제량백려호순조지간차이무통계학의의(0.928±0.021여0.908±0.026);고제량백려호순조저우백작총감조급저제량백려호순조(0.507±0.01여0.525±0.015,0.908±0.026,P<0.01);LEF조저우고、중제량백려호순조(0.391±0.026여0.507±0.010,0.570±0.021,P<0.01).결론 ①고、중제량백려호순능구완해CIA적염증증상,이저제량백려호순칙무차작용.②중등제량백려호순대CIA대서적단기료효여TGP상당,고제량백려호순적료효강우TGP,단약우LEF.③백려호순능구억제혈청항CⅡ항체적생성.
Objective To investigate the anti-inflammatory effect of Resveratrol on type Ⅱ collagen induced arthritis.Methods Collagen induced arthritis (CIA) animal model was established by subcutaneous injection of type Ⅱ collagen emulsified with incomplete and complete Freud's adjuvant to Wistar rats.Fortytwo rats were successfully induced and randomly divided into 7 groups:the experimental group (A),the leflunomide treatment group (B),the TGP treatment group (C),the methotrexate group (D),the low dose Resveratrol group (E),the medium dose Resveratral group (F) and high dose Resveratrol group (G) and the normal control group (H).Symptoms of arthritis were recorded and selalm levels of the anti-C Ⅱ antibody were detected by ELISA.Results For arthritis index.there was no significant difference between groups E and A,neither between groups C and F.The arthritis index was lower in group G than group C,but both of them were higher than groups B and D.② For serum anti-C Ⅱ antibody level,that of group A was higher than groups B,C,D,F and G.There was no difference between groups A and E,and groups C and F.That of Group G was lower than groups C and E.Conclusion High and medium dose of Resveratrol can relieve foot joints swelling in the CIA rats,but low dose does not have similar effect.The effect of medium dose of Resveratrol iS similar to TGP,but weaker than that of leflunomide.Resveratrol may conduct its anti-inflammatory effect via lowering the concentration of the anti-C Ⅱ antibody in the serum.