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通痹灵对抗胶原诱导性关节炎小鼠骨质破坏的作用研究 被引量:5

Effects of Tongbiling Prescription in Counteracting Bone Destruction in Rats with Collagen-induced Arthritis
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摘要 [目的]探讨通痹灵(TBL)抗关节炎骨质破坏的作用机理。[方法]以小鼠胶原诱导性关节炎(CIA)为动物模型,分别以高剂量和低制量TBL对模型小鼠灌胃给药,并以甲氨喋呤(MTX)作为阳性对照,观察TBL对CIA小鼠关节炎症程度、关节破坏程度以及关节切片免疫组化染色中明胶酶A和B表达的影响。[结果](1)TBL高剂量(5.7g·kg-1·d-1)治疗8周能降低关节炎症状计分及放射线计分(P<0.01或P<0.001);(2)明胶酶A和B表达与关节炎症状计分及关节放射线计分显著相关(P<0.05或P<0.005);(3)TBL高剂量治疗能明显降低明胶酶A和B在关节滑膜、软骨和滑膜翳中的表达(与CIA组相比P<0.01或P<0.001)。[结论]中药TBL可控制CIA小鼠关节明胶酶A和B的表达,这可能是其能改善RA的软骨和骨质破坏的机制之一。 [Objective] To explore the mechanism of Tongbiling (TBL) prescription in counteracting cartilage destruction in mice with rheumatoid arthritis (RA). [Methods] Collagen-induced arthritis (CIA) rat models were medicated with gastric infusion of high-dose and low-dose TBL and methotrenxate (MTX) respectively and then the effects of TBL on articular inflammation and destruction were observed and gelatinase A and B expression was examined by immunolocalization. [Results] (1) Administration of TBL (5.7 g kg-1 d-1 ) for 8 weeks after first immunization decreased clinical scores (CS) and radiological scores (RS) (P < 0.01 or P < 0.001); (2) the degree and the density of gelatinase A and B expression were markedly correlated with clinical scores and radiological scores ( P < 0.05 or P < 0.005); (3) the expressions of gelatinase A and B were dramatically suppressed in synovium, cartilage and cartilage-pannus of high-dose (5.7gkg-1 d-1) TBL group (P < 0.01 or P < 0.001 as compared with CIA model group). [Conclusion] The regulatory actions of TBL on the expressions of gelatinase A and B may be one of the mechanisms of TBL in counteracting the destruction of bone and cartilage.
出处 《广州中医药大学学报》 CAS 2003年第1期13-17,共5页 Journal of Guangzhou University of Traditional Chinese Medicine
基金 国家自然科学基金重点项目资助(编号:960550 39930230)
关键词 类风湿关节炎 中药疗法 通痹灵 药理学 桂枝芍药知母汤 金属蛋白酶类 ARTHRITIS, RHEUM ATOID/TCD therapy TONGBILING/pharmacology GUIZHI SHAOYAO ZHIMU DECOCTION/pharmacology METALLOPROTEINASES
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  • 1[美]吉尔曼(Gilman,A·G·)等 著,谭世杰.治疗学的药理基础[M]人民卫生出版社,1987. 被引量:1

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