CAJ | 학술논문

目的：观察基质金属蛋白酶1( MMP-1)及其抑制剂(TIMP-1)在白藜芦醇治疗佐剂性关节炎(AA)的滑膜组织和关节软骨中的表达,探讨MMP-1及TIMP-1的异常表达是否参与AA的发病机制。方法60只SD大鼠随机分为2组：正常组(10只),模型组(50只)。模型组弗氏完全佐剂注射诱导关节炎12 d后,在其足趾出现继发性免疫炎症反应时,又随机分成4组：模型对照组、白藜芦醇低剂量组(5 mg/kg)、白藜芦醇高剂量组(15 mg/kg)、阳性对照雷公藤多苷组(100 mg/kg)。大鼠每天均灌胃给予溶媒或药物,持续16 d后处死大鼠；免疫组化法检测滑膜组织MMP-1、TIMP-1表达；滑膜组织匀浆,Western blot法检测MMP-1、TIMP-1蛋白含量。结果白藜芦醇能明显抑制模型组大鼠病理损害程度,模型组滑膜组织MMP-1、TIMP-1高表达,白藜芦醇治疗组能抑制MMP-1、TIMP-1的高表达,在抗关节炎的作用上有相关性。结论白藜芦醇具有抑制AA大鼠的炎症作用,防止关节退变的病理变化,其机制与调节大鼠的基质金属蛋白酶在滑膜组织和关节软骨的表达有关。
목적：관찰기질금속단백매1( MMP-1)급기억제제(TIMP-1)재백려호순치료좌제성관절염(AA)적활막조직화관절연골중적표체,탐토MMP-1급TIMP-1적이상표체시부삼여AA적발병궤제。방법60지SD대서수궤분위2조：정상조(10지),모형조(50지)。모형조불씨완전좌제주사유도관절염12 d후,재기족지출현계발성면역염증반응시,우수궤분성4조：모형대조조、백려호순저제량조(5 mg/kg)、백려호순고제량조(15 mg/kg)、양성대조뢰공등다감조(100 mg/kg)。대서매천균관위급여용매혹약물,지속16 d후처사대서；면역조화법검측활막조직MMP-1、TIMP-1표체；활막조직균장,Western blot법검측MMP-1、TIMP-1단백함량。결과백려호순능명현억제모형조대서병리손해정도,모형조활막조직MMP-1、TIMP-1고표체,백려호순치료조능억제MMP-1、TIMP-1적고표체,재항관절염적작용상유상관성。결론백려호순구유억제AA대서적염증작용,방지관절퇴변적병리변화,기궤제여조절대서적기질금속단백매재활막조직화관절연골적표체유관。
Objective To investigate the expression of matrix metalloproteinases 1 ( MMP-1 ) and tissue matrix metalloproteinases inhibitor-1 ( TIMP-1 ) of synovial tissues and articular cartilage in rats with adjuvant arthritis (AA),to explore whether there is a relation between pathogenesis of AA and expression of MMP-1 and TIMP-1. Methods 60 SD rats were randomly divided into 2 groups:normal control group ( n=10 ) and model group ( n=50). The model group was injected freund's complete adjuvant induced arthritis. When the right paw was induced af-ter 12 days and secondary immune-inflammatory feet were swelled,the rats were randomly divided into 4 groups, and each group had 10 rats:model,resveratrol low dose group(5 mg/kg) , resveratrol high dose group(15 mg/kg) , positive control tripterygium wilfordii glycoside ( TWG, 100 mg/kg ) , qd × 18 day;after inducing inflammatory paw, the expressions of MMP-1 and TIMP-1 in synovial tissue and articular cartilage were detected by immunohis-toehemistry. MMP-1 and TIMP-1 protein content in synovial tissue was detected by Western blot. Results Res-veratrol could inhibit model group rats pathological damage, compared with the AA model group, synovial tissue ex-pression of MMP-1 was significantly higher in resveratrol-treated groups ( P<0 . 05 , P<0. 01 ) , the expression of TIMP-1 was also higher ( P<0. 05 ) . There was a correlation in the role of the anti-inflammation. Conclusion Resveratrol inhibits the inflammation of AA rats and prevents the pathological changes of the joint degeneration, its mechanism is related to regulation of matrix metalloproteinases in synovial tissue of rats and the expression of articu-lar cartilage.