风湿病与关节炎
風濕病與關節炎
풍습병여관절염
Rheumatism and Arthritis
2015年
1期
9-13
,共5页
徐轶尔%孙贵才%郑春雨%吴洪亮%刘明海%凌小鹏%孙步蟾%涂远青%樊祥伟
徐軼爾%孫貴纔%鄭春雨%吳洪亮%劉明海%凌小鵬%孫步蟾%塗遠青%樊祥偉
서질이%손귀재%정춘우%오홍량%류명해%릉소붕%손보섬%도원청%번상위
痛风性关节炎%豨莶草%尿酸钠%IL-1β%TNF-α%NF-κB%大鼠
痛風性關節炎%豨薟草%尿痠鈉%IL-1β%TNF-α%NF-κB%大鼠
통풍성관절염%희렴초%뇨산납%IL-1β%TNF-α%NF-κB%대서
gouty arthritis%Xixiancao%sodium urate%IL-1β%TNF-α%NF-κB%rat
目的：研究豨莶草对尿酸钠引起的痛风性关节炎细胞炎性因子的作用机制。方法：选取健康清洁级10～13周龄雄性Wistar大鼠108只，随机分为空白对照组、模型对照组、莶草高剂量组、莶草中剂量组、莶草低剂量组、秋水仙碱组，每组18只。除空白对照组外，其余各组均通过尿酸钠致大鼠痛风性关节炎模型，用莶草不同剂量和秋水仙碱对模型大鼠灌胃给药。观察各组大鼠关节组织的病理学变化和测定白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）、核转录因子-κB（NF-κB）的表达。结果：模型对照组大鼠膝关节红肿明显且不敢发力，肿胀关节浸出液中IL-1β、TNF-α、NF-κB水平显著升高，滑膜细胞增生、炎性细胞浸润，排列紊乱，成纤维细胞增生，组织坏死并且炎性渗出。莶草高、中剂量组治疗效果明显，红肿减弱，莶草高剂量组周围软组织中炎细胞浸润并不明显，肿胀关节浸出液中IL-1β、TNF-α、NF-κB均显著降低。结论：莶草通过抑制IL-1β、TNF-α、NF-κB表达，可有效抑制痛风性关节炎局部的炎症反应。
目的：研究豨薟草對尿痠鈉引起的痛風性關節炎細胞炎性因子的作用機製。方法：選取健康清潔級10～13週齡雄性Wistar大鼠108隻，隨機分為空白對照組、模型對照組、薟草高劑量組、薟草中劑量組、薟草低劑量組、鞦水仙堿組，每組18隻。除空白對照組外，其餘各組均通過尿痠鈉緻大鼠痛風性關節炎模型，用薟草不同劑量和鞦水仙堿對模型大鼠灌胃給藥。觀察各組大鼠關節組織的病理學變化和測定白細胞介素-1β（IL-1β）、腫瘤壞死因子-α（TNF-α）、覈轉錄因子-κB（NF-κB）的錶達。結果：模型對照組大鼠膝關節紅腫明顯且不敢髮力，腫脹關節浸齣液中IL-1β、TNF-α、NF-κB水平顯著升高，滑膜細胞增生、炎性細胞浸潤，排列紊亂，成纖維細胞增生，組織壞死併且炎性滲齣。薟草高、中劑量組治療效果明顯，紅腫減弱，薟草高劑量組週圍軟組織中炎細胞浸潤併不明顯，腫脹關節浸齣液中IL-1β、TNF-α、NF-κB均顯著降低。結論：薟草通過抑製IL-1β、TNF-α、NF-κB錶達，可有效抑製痛風性關節炎跼部的炎癥反應。
목적：연구희렴초대뇨산납인기적통풍성관절염세포염성인자적작용궤제。방법：선취건강청길급10～13주령웅성Wistar대서108지，수궤분위공백대조조、모형대조조、렴초고제량조、렴초중제량조、렴초저제량조、추수선감조，매조18지。제공백대조조외，기여각조균통과뇨산납치대서통풍성관절염모형，용렴초불동제량화추수선감대모형대서관위급약。관찰각조대서관절조직적병이학변화화측정백세포개소-1β（IL-1β）、종류배사인자-α（TNF-α）、핵전록인자-κB（NF-κB）적표체。결과：모형대조조대서슬관절홍종명현차불감발력，종창관절침출액중IL-1β、TNF-α、NF-κB수평현저승고，활막세포증생、염성세포침윤，배렬문란，성섬유세포증생，조직배사병차염성삼출。렴초고、중제량조치료효과명현，홍종감약，렴초고제량조주위연조직중염세포침윤병불명현，종창관절침출액중IL-1β、TNF-α、NF-κB균현저강저。결론：렴초통과억제IL-1β、TNF-α、NF-κB표체，가유효억제통풍성관절염국부적염증반응。
Objective:To research the mechanism of action of Xixiancao[Herba Siegesbeckiae] to the cell inlfammatory factor of gouty arthritis induced by sodium urate.Methods: 108 Wistar male rats of clean grade 10-13 weeks were randomly divided into blank control group,model control group,Xixiancao high dose group,Xixiancao middle dose group group,Xixiancao low dose group and colchicine group,18 rats in each group. Except for the blank control group,the other groups by gouty arthritis rat model induced by sodium urate.The models were given different dosage of Xixiancao and colchicine by intragastric administration,observing their pathological changes of articular tissue and measuring the expression of IL-1β,TNF-α and NF-κB.Results:The rats in the model control group had knee joint swelling obviously and couldn’t move with force.The level of IL-1β, TNF-α and NF-κB in the leachate form the swollen joints signiifcantly increased.There were synovial cell hyper-plasia,inlfammatory cell inifltration,arrangement in disorder,ifbroblast proliferation,tissue necrosis and inlfammato-ry exudation.The therapeutic effect of the high and middle dose groups of Xixiancao was obvious and red swelling weakened.The phlogocyte inifltration in sur-rounding soft tissue of the high dose group of Xixiancao was not obvious and IL-1β, TNF-α and NF-κB in the leachate form the swollen joints signiifcantly decreased.Conclusion:By the expression of IL-1β,TNF-α and NF-κB,Xixiancao could effectively inhibit the local inlfammatory reaction of gouty arthritis.
