摘要
目的:从滑膜新生血管生成的角度,部分揭示祛痹方治疗类风湿关节炎(RA)的作用机制。方法:选用雄性SD大鼠,随机选取12只作为空白对照组,其余60只采用尾根部皮下注射Ⅱ型胶原与不完全弗氏佐剂的方法制作胶原诱导性关节炎(CIA)模型。15d后将CIA大鼠随机分为模型组、雷公藤多苷组、祛痹方高、低剂量组,随即灌胃给药,1次/d,连续4周。采用免疫组化的方法检测大鼠膝关节滑膜组织中fins样酪氨酸激酶(FLT-4)和胎肝激酶受体(FLK-1)的变化。结果:与空白对照组比较,模型组大鼠FLK-1、FLT-4明显升高(P<0.01);雷公藤多苷组和祛痹方高剂量组FLK-1、FLT-4水平较模型组明显降低(P<0.01),且祛痹方高剂量组FLK-1较雷公藤多苷组明显降低(P<0.05)。结论:祛痹方治疗RA的功效与抑制新生血管生成相关。
Objective: From the perspective of synovial angiogenesis, to investigate the mechanism of Qubi Recipe in the treatment of rheumatoid arthritis(RA). Methods: Twelve male SD rats were randomly selected as blank control group, and 60 male SD rats were established as experiment arthritis rat model by subcutaneous injection of Ⅱ collagen and non-complete Freunds adjuvant. After 15 days, 60 CIA rats were randomly divided into model group, tripterygium glycosides group, Qubi Recipe high and low-dose groups. The rats in the treatment groups were administered intragastrically every day, for 4 weeks. The changes offins-like tyrosine kinase(FLT-4) and fetal liver kinase receptor(FLK-1) on synovial tissues in knee were detected by immunohistochemistry method. Results: Compared with the blank control group, the expression of FLK-1 and FLT-4 were obviously increased(P〈0.01). The level of FLK-1 and FLT-4 were decreased in tripterygium glycosides group and Qubi Recipe high-dose group(P〈0.01). Moreover, the expression of FLK-1 in Qubi Recipe high-dose group was signii cantly lower than those in tripterygium glycosides group(P〈0.05). Conclusion: The treatment effect of Qubi Recipe for RA is correlated with theinhibition of angiogenesis.
出处
《中华中医药杂志》
CAS
CSCD
北大核心
2014年第7期2312-2314,2071,共3页
China Journal of Traditional Chinese Medicine and Pharmacy
基金
国家重大新药创制科技重大专项(No.2009ZX09502-019)
国家科技支撑计划重点课题(No.2006BAI08B01-01)~~
关键词
祛痹方
胶原诱导性关节炎
滑膜血管生成调控因子
fins样酪氨酸激酶
胎肝激酶受体
Qubi Recipe
TypeⅡ collagen-induced arthritis
Synovial vascular generate regulatory factors
Fins-like tyrosine kinase
Fetal liver kinase receptor