环球中医药
環毬中醫藥
배구중의약
GLOBAL TCM
2015年
6期
692-696
,共5页
柳洋%朱跃兰%侯秀娟%刘小平
柳洋%硃躍蘭%侯秀娟%劉小平
류양%주약란%후수연%류소평
缺氧诱导因子1α%血管生成素1%血管生成素2%胶原诱导性关节炎%血管新生
缺氧誘導因子1α%血管生成素1%血管生成素2%膠原誘導性關節炎%血管新生
결양유도인자1α%혈관생성소1%혈관생성소2%효원유도성관절염%혈관신생
HyPoxia-inducible factor-1α%AngioPoietin-1%AngioPoietin-2%Collagen-in-duced arthritis%Angiogenesis
目的:观察芍甘附子汤加味对胶原诱导性关节炎大鼠滑膜组织缺氧诱导因子1α( hy-poxia-inducible factor-1α,HIF-1α)、血管生成素1(angiopoietin-1,Ang-1)和血管生成素2(angiopoietin-2,Ang-2)的影响,探讨其治疗类风湿关节炎的抗血管新生作用机制。方法选用健康Wistar大鼠30只,随机分为正常组、模型组、对照组(雷公藤多甙片组)和小、中、大剂量治疗组(芍甘附子汤加味组),除正常组均制备胶原诱导性关节炎( Collagen-induced arthritis, CIA)模型,造模成功后连续给药28天。测定各组大鼠足趾肿胀体积,进行关节炎指数( Arthritis index, AI)评分,采用免疫组织化学方法检测大鼠膝关节滑膜组织HIF-1α、Ang-1和Ang-2的表达。结果与模型组比较,对照组和大剂量治疗组足趾肿胀体积有所降低(P<0.05),对照组和中、大剂量治疗组AI评分明显降低(P<0.01);与正常组比较,模型组HIF-1α和Ang-1表达均显著升高(P<0.01),Ang-2表达有所升高(P<0.05);与模型组比较,对照组和大、中剂量治疗组 HIF-1α和 Ang-1表达均出现显著降低( P<0.01),Ang-2表达呈降低趋势。结论芍甘附子汤加味可能通过降低类风湿关节炎滑膜组织HIF-1α、Ang-1和Ang-2的表达,抑制滑膜血管新生,从而起到治疗类风湿关节炎的作用。
目的:觀察芍甘附子湯加味對膠原誘導性關節炎大鼠滑膜組織缺氧誘導因子1α( hy-poxia-inducible factor-1α,HIF-1α)、血管生成素1(angiopoietin-1,Ang-1)和血管生成素2(angiopoietin-2,Ang-2)的影響,探討其治療類風濕關節炎的抗血管新生作用機製。方法選用健康Wistar大鼠30隻,隨機分為正常組、模型組、對照組(雷公籐多甙片組)和小、中、大劑量治療組(芍甘附子湯加味組),除正常組均製備膠原誘導性關節炎( Collagen-induced arthritis, CIA)模型,造模成功後連續給藥28天。測定各組大鼠足趾腫脹體積,進行關節炎指數( Arthritis index, AI)評分,採用免疫組織化學方法檢測大鼠膝關節滑膜組織HIF-1α、Ang-1和Ang-2的錶達。結果與模型組比較,對照組和大劑量治療組足趾腫脹體積有所降低(P<0.05),對照組和中、大劑量治療組AI評分明顯降低(P<0.01);與正常組比較,模型組HIF-1α和Ang-1錶達均顯著升高(P<0.01),Ang-2錶達有所升高(P<0.05);與模型組比較,對照組和大、中劑量治療組 HIF-1α和 Ang-1錶達均齣現顯著降低( P<0.01),Ang-2錶達呈降低趨勢。結論芍甘附子湯加味可能通過降低類風濕關節炎滑膜組織HIF-1α、Ang-1和Ang-2的錶達,抑製滑膜血管新生,從而起到治療類風濕關節炎的作用。
목적:관찰작감부자탕가미대효원유도성관절염대서활막조직결양유도인자1α( hy-poxia-inducible factor-1α,HIF-1α)、혈관생성소1(angiopoietin-1,Ang-1)화혈관생성소2(angiopoietin-2,Ang-2)적영향,탐토기치료류풍습관절염적항혈관신생작용궤제。방법선용건강Wistar대서30지,수궤분위정상조、모형조、대조조(뢰공등다대편조)화소、중、대제량치료조(작감부자탕가미조),제정상조균제비효원유도성관절염( Collagen-induced arthritis, CIA)모형,조모성공후련속급약28천。측정각조대서족지종창체적,진행관절염지수( Arthritis index, AI)평분,채용면역조직화학방법검측대서슬관절활막조직HIF-1α、Ang-1화Ang-2적표체。결과여모형조비교,대조조화대제량치료조족지종창체적유소강저(P<0.05),대조조화중、대제량치료조AI평분명현강저(P<0.01);여정상조비교,모형조HIF-1α화Ang-1표체균현저승고(P<0.01),Ang-2표체유소승고(P<0.05);여모형조비교,대조조화대、중제량치료조 HIF-1α화 Ang-1표체균출현현저강저( P<0.01),Ang-2표체정강저추세。결론작감부자탕가미가능통과강저류풍습관절염활막조직HIF-1α、Ang-1화Ang-2적표체,억제활막혈관신생,종이기도치료류풍습관절염적작용。
Objective The Purpose of the present study was to examine the effects of modified Shaogan Fuzi Decoction on the expressions of hypoxia-inducible factor-1α ( HIF-1α) , angiopoietin-1 (Ang-1) and angiopoietin-2(Ang-2) in the synovial tissue of rats with collagen-induced arthritis (CIA), and to investigate the anti-angiogenesis mechanism of modified Shaogan Fuzi Decoction in treating rheuma-toid arthritis( RA) . Methods Thirty healthy female Wistar rats were randomly divided into 6 groups:con-tral group, model group, tripterygium glucoside group and low, middle and high dose treatment group of modified Shaogan Fuzi Decoction. After the CIA rat model was successfully established, rats were intragas-trically administrated with distilled water in the control group or medicine in the treatment groups for twenty-eight days. The toe swell volume was measured;the arthritis index ( AI) was evaluated and the expression levels of HIF-1α, Ang-1 and Ang-2 were observed by immunohistochemical staining. Results Compared to that of in the model group, the toe swell volume of the tripterygium glucoside group and the high dose group significantly reduced (P<0. 05);the AI score of the tripterygium glucoside group and the middle, high dose groups significantly reduced compared to the model group (P<0. 01); Compared to the control group, the expression levels of HIF-1α, Ang-1 and Ang-2 significantly reduced in the model group (P<0. 01, P<0. 05);the expression levels of HIF-1αand Ang-1 significantly decreased in the tripterygium glu-coside group and the high and middle groups compared to the model group (P<0. 01), and Ang-2 expres-sion showed a downward trend. Conclusion The experimental data implied that modified Shaogan Fuzi Decoction plays an important role in treating RA via the way of inhibiting angiogenesis in synovial tissue by down-regulating the expressions of HIF-1α, Ang-1 and Ang-2.