葡萄酒协同洋葱对大鼠痛风症作用的研究

目的通过尿酸钠(monosodium urate monohydrate,MSU)晶体诱导炎症动物模型,探讨红酒泡洋葱对急性痛风性关节炎(acute gouty arthritis,GA)的治疗作用。方法选用48只健康雄性SD大鼠,随机分为6组:空白组,模型组,阳性组,葡萄酒协同洋葱低剂量组,葡萄酒协同洋葱中剂量组和葡萄酒协同洋葱高剂量组。采用MSU晶体制备大鼠GA模型。空白组和模型组给予生理盐水,阳性组给予雷公藤多苷片,低、中、高剂量组分别给予不同剂量的葡萄酒+洋葱,检测血清中UA、IL-1β和CAT活性水平。取踝关节滑膜,观测其病理变化。结果低剂量(3mg·kg-1)能够显著降低GA模型大鼠的踝关节肿胀度及白细胞介素浓度(P<0.01),提高CAT活性(P<0.01);低、中(6mg·kg-1)剂量能够显著降低血清中尿酸的含量(P<0.01);尿酸钠所致痛风症大鼠的关节滑膜病变显著,经给药后各组大鼠的关节滑膜病理情况均有所缓解。结论葡萄酒泡洋葱可降低MSU晶体诱导的GA大鼠血清中尿酸及白细胞介素的水平,增强过氧化氢酶活性,对关节滑膜有保护和修复作用,其机制可能与抗氧化作用有关。     

金关片对大鼠痛风性关节炎的药效作用研究

目的 探讨金关片对大鼠痛风性关节炎的药效作用.方法 采用尿酸钠晶体制备大鼠痛风性关节炎模型,分别测量大鼠足肿胀度,血清中尿酸(UA)和一氧化氮(N0)的水平及大鼠踝关节软组织中炎症因子(IL-1、IL-6、TNF-α)的含量.结果 金关片能显著降低痛风性关节炎模型大鼠踝关节的容积(P ＜0.05、P＜0.01),降低血清中UA、NO的水平(P＜0.05、P＜0.01)以及关节软组织中IL-1、IL-6、TNF-α的水平(P ＜0.05、P＜0.01).结论 金关片对大鼠痛风性关节炎具有防治作用,其抗炎的机制可能与其降低炎症组织中IL-1、IL-6、TNF-α的含量,减轻其炎症损害有关.     

萆薢总皂苷对大鼠急性痛风性关节炎NALP3炎性体信号通路的影响

目的研究萆薢总皂苷对大鼠急性痛风性关节炎的防治作用及机制。方法 Wistar大鼠,♂,72只,随机分组后,各用药组大鼠预先灌胃给予不同剂量萆薢总皂苷,随后右侧踝关节腔注射尿酸钠诱导急性痛风性关节炎。观察大鼠步态,测定关节肿胀度,HE染色进行病理学分析。ELISA法检测血清TNF-α、IL-1β、IL-18表达。Western blot法检测滑膜组织中pro-IL-1β、NALP3炎性体相关蛋白变化。结果萆薢总皂苷各浓度和秋水仙碱均可改善大鼠步态。TSD高、中剂量组与秋水仙碱类似,可降低大鼠关节肿胀度,病理学检查踝关节病变好转,血清TNF-α、IL-1β、IL-18明显减少,滑膜组织pro-IL-1β、NALP3、ASC、caspase-1前体和活性形式蛋白表达降低。结论萆薢总皂苷对大鼠急性痛风性关节炎具有防治作用,机制可能是抑制NALP3炎性体装配和激活,以及抑制炎性细胞因子的表达。     

N-9,10-蒽醌-2-甲酰基苯丙氨酸治疗大鼠痛风性关节炎的作用及机制

目的 探究N-9,10-蒽醌-2-甲酰基苯丙氨酸(NAY)对尿酸钠(MSU)所致痛风性关节炎(GA)大鼠的作用及机制。方法 将雄性SD大鼠随机分为7组,每组8只,即正常组、模型组、NAY低(20 mg·kg^-1)、中(40 mg·kg^-1)、高剂量组(80 mg·kg^-1)、秋水仙碱组(0.8 mg·kg^-1)和别嘌呤醇组(10 mg·kg^-1),通过关节腔内注射MSU晶体建立大鼠急性GA模型,各组灌胃给药5 d,给药第3天造模。将原代培养的大鼠腹部巨噬细胞分成空白组、模型组、NAY组、MCC950组和联合给药组。软尺测量大鼠踝关节周长并计算大鼠关节肿胀度;检测大鼠血清尿酸(UA)、肌酐(CRE)和尿素氮(BUN)含量;HE染色观察大鼠踝关节滑膜组织病理切片;检测各组血清、关节滑膜和细胞上清液中肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)的含量;并检测各组关节滑膜和细胞中NOD样受体热蛋白结构域相关蛋白3(NLRP3)、凋亡相关斑点样蛋白(ASC)和半胱氨酸天冬氨...     

藤茶提取物中二氢杨梅素对大鼠急性痛风性关节炎模型的影响

目的研究藤茶提取物中二氢杨梅素对大鼠急性痛风性关节炎模型中血清IL-1β、IL-8、TNF-α的影响,初步探讨其治疗急性痛风性关节炎的作用机制。方法采用踝关节腔内注射尿酸钠建立急性痛风性关节炎大鼠模型,以秋水仙碱为对照,观察藤茶提取物中二氢杨梅素对各组大鼠的踝关节肿胀度及血清TNF-α、IL-1β及IL-8水平的调节作用。结果模型组关节肿胀度、IL-1β、IL-8和TNF-α的水平明显高于空白对照组(P<0.05或P<0.01);中高剂量的二氢杨梅素能明显抑制急性痛风性关节炎大鼠的踝关节肿胀度,降低血清TNF-α、IL-1B及IL-8的水平。结论藤茶提取物中二氢杨梅素对急性痛风性关节炎具有良好的治疗作用,其作用机制与抑制血清IL-1β、IL-8和TNF-α的产生有关。     

四妙勇安方水提物对大鼠急性痛风性关节炎的治疗作用及其对外周血 IL-1β、TNF-α和 MIF 水平的影响

目的：探讨四妙勇安方水提物（SMYA）对急性痛风性关节炎（ AGA）大鼠的治疗作用及其对血清巨噬细胞移动抑制因子（MIF）、白介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）水平的影响。方法将40只 SD 雄性大鼠随机分为4组：SMYA 组、秋水仙碱（COL）组、模型组、正常组,每组10只。SMYA 组与 COL 组每日分别予 SMYA 相当于生药1 g / kg、COL 0.8 mg / kg 灌胃,模型组与正常组每日给予等量生理盐水灌胃。药物干预第5天,于模型组、COL 组、SMYA 组大鼠左踝关节腔注射 PBS 配制的微晶尿酸钠结晶（25 mg / ml）100μl,复制 AGA 模型。分别于造模后1、2、4、6、8、12、24 h 使用游标卡尺记录每组大鼠踝关节肿胀程度。造模后24 h 对各组大鼠腹主动脉采血,离心,留取血清,采用酶联免疫吸附实验（ELISA）检测血清 MIF、IL-1β、TNF-α水平。结果 SMYA 组、COL 组及模型组踝关节肿胀度均于造模后8 h 达到高峰,之后缓慢下降。造模后4、6、8、12、24 h SMYA 组、COL 组及模型组踝关节肿胀度显著高于正常组（P ﹤0.05）,SMYA 组和 COL 组踝关节肿胀度显著低于模型组（ P ﹤0.05）,上述差异以8 h 时更为显著（ P ﹤0.01）;造模后12、24 h SMYA 组踝关节肿胀度显著低于 COL 组（P ﹤0.05）。与模型组比较,SMYA 组、COL 组 MIF、IL-1β、TNF-α表达显著减弱（P ﹤0.05）;与 COL 组比较,SMYA 组 MIF、IL-1β表达更强,TNF-α表达更弱（ P ﹤0.05）。结论 SMYA 对大鼠 AGA 具有显著治疗效应,其作用机制与抑制促炎细胞因子 MIF、IL-1β、TNF-α的表达有关。     

伸筋草生物碱对佐剂性关节炎大鼠的抗炎作用及机制研究

目的 探讨伸筋草生物碱对完全弗氏佐剂（CFA）诱导大鼠关节炎的治疗作用及机制。方法 健康SD大鼠48只,随机分为6组,每组8只,即对照组、模型组、依托考昔片（阳性药,1 mg/kg）组及伸筋草生物碱低、中、高剂量（30、60、120 mg/kg）组,除对照组外,其余40只大鼠sc 0.1 mL CFA造模,致炎15 d后,连续ig给药30 d。测定大鼠足趾肿胀率、HE染色后观察造模测踝关节滑膜病理改变;致炎45 d,ELISA法测定血清中白介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）水平。结果 与模型组比较,依托考昔片及伸筋草生物碱低、中、高剂量组足趾肿胀率均显著下降（P<0.05、0.01）;中、高剂量伸筋草生物碱明显改善滑膜细胞、巨噬细胞、纤维细胞增生与炎症细胞浸润;与模型组比较,依托考昔片及伸筋草生物碱高剂量组大鼠血清TNF-α水平显著下降（P<0.05）,依托考昔片及伸筋草生物碱各剂量组IL-1β水平均显著降低（P<0.01）。结论 伸筋草生物碱显著抑制CFA诱导关节炎大鼠关节肿胀,改善大鼠踝关节滑膜病变,其作用机制可能与降低体内IL-1β、TNF-α水平有关。     

荣骨定痛膏对骨性关节炎模型大鼠炎性细胞及细胞因子的影响

目的 研究荣骨定痛膏对骨性关节炎模型大鼠炎性细胞及细胞因子的影响。方法 采用注射4%木瓜蛋白酶复制骨性关节炎大鼠模型,观测膝关节功能、关节滑膜厚度和关节滑液中炎性细胞数,酶联免疫法检测血清IL-1β、IL-6、TNF-α。结果 荣骨定痛膏可明显减小骨性关节炎大鼠关节滑膜肿胀厚度,扩大膝关节的活动范围,减少关节滑液中炎性细胞数,降低血清IL-1β、IL-6与TNF-α的水平。结论 荣骨定痛膏对骨性关节炎具有一定的治疗作用,缓解关节炎症、降低IL-1β、IL-6、TNF-α水平可能是其作用机制之一。     

痛风宁对尿酸钠致大鼠关节炎滑膜IL-1、IL-6含量的影响

目的：通过观察痛风宁对尿酸钠致大鼠关节炎滑膜组织IL-1、IL-6含量的影响，研究其对急性痛风的抗炎作用。方法：通过尿酸钠溶液注入大鼠踝关节造成急性痛风模型。痛风宁药液、秋水仙碱悬浮液灌胃给药，均为每次4ml，每天2次，连续5天。取受试关节滑膜组织测定IL-1、IL-6的含量。结果：动物造模后，关节滑膜组织IL-1、IL-6含量均明显升高，中药能明显降低IL-1、IL-6含量，与模型组比较均有非常显著性差异(P≤0．01)。结论：尿酸钠致大鼠关节炎滑膜组织IL-1、IL-6均升高，而痛风宁能使实验性急性痛风滑膜组织IL-1、IL-6含量明显下降，说明痛风宁可能通过抑制滑膜细胞IL-1、IL-6的合成，进而抑制PEG2等其他炎症介质的释放而发挥抗炎镇痛作用，但其对急性痛风滑膜细胞的调控机理有待进一步研究。     

新风胶囊对佐剂性关节炎模型大鼠的抗炎作用

目的:研究新风胶囊对佐剂性关节炎(AA)模型大鼠的抗炎作用。方法:取70只SD大鼠随机均分为正常对照组、模型对照(等容生理盐水)组、阳性对照中药[祛风止痛胶囊0.4 g(生药)/kg]组、阳性对照西药(来氟米特片2.1 mg/kg)组和新风胶囊低、中、高剂量[0.8、1.6、3.2 g(生药)/kg]组,依次记为A、B、C、D、E、F、G组,除A组外其余各组大鼠皮内注射弗氏完全佐剂复制AA模型,致炎第12天开始连续ig给药28 d。检测并计算各组大鼠给药前、后足趾肿胀度和关节炎指数,于末次给药24 h后检测各组大鼠血清及关节滑膜组织中白细胞介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)含量并观察踝关节组织病理学形态变化。结果:与A组比较,B组大鼠足趾肿胀度和关节炎指数升高,血清及关节滑膜组织中IL-1β、TNF-α含量增加,差异有统计学意义(P<0.01)。与给药前比较,C、D、E、F、G组大鼠足跖肿胀度和关节炎指数降低,差异有统计学意义(P<0.05)。与B组比较,C、D、E、F、G组大鼠足趾肿胀度和关节炎指数降低,血清及关节滑膜组织中IL-1β、TNF-α含量降低,差异有统计学意义(P<0.01或P<0.05)。B组大鼠踝关节组织出现滑膜增生、炎性细胞浸润;C、D、F、G组大鼠滑膜增生和炎症情况较B组均减轻。结论:新风胶囊对AA模型大鼠具有抗炎作用,其机制可能与促进滑膜细胞凋亡、抑制滑膜增生有关。     

Therapeutic properties of quercetin on monosodium urate crystal-induced inflammation in rat

Objectives Gouty arthritis is characterized by intense, acute inflammatory reactions that occur in response to articular deposits of monosodium urate crystals. In this study we have assessed the effects of the flavonoid, quercetin, on monosodium urate crystal‐induced inflammation in rats, an experimental model for gouty arthritis. Methods Gouty arthritis was induced by intra‐articular injection of monosodium urate crystal suspension inside the ankle joint of the rat right hind limb. Circumference was assessed at 2, 4, 8, 12, 24, and 48 h after monosodium urate crystal injection. Histopathological analysis of joint synovial tissue, inflammatory mediator levels, lipid peroxidation, and antioxidant status in serum, liver and joint synovial tissue were determined in control and monosodium urate crystal‐treated rats at the end of experiment. Key findings Quercetin treatment attenuated oedema in a dose‐dependent manner and decreased histological signs of acute inflammation in the treated animals. In addition, quercetin treatment suppressed leucocyte recruitment, decreased chemokine levels, decreased levels of the lipid peroxidation end‐product malondialdehyde, and increased antioxidant enzyme activity in treated rats. Conclusions These results indicated that quercetin exerted a strong anti‐inflammatory effect that may be useful for the treatment of acute gouty arthritis.     

痛风颗粒抗炎降尿酸作用的实验研究

目的:通过痛风颗粒对大鼠痛风性关节炎及痛风性高尿酸血症防治作用的实验研究,初步探究其药效学作用。方法:采用微晶型尿酸钠(monosodium urate,MSU)致大鼠踝关节肿胀、足跖肿胀模型和尿酸(uric acid,UA)诱导大鼠高尿酸血症模型,测定大鼠足肿胀率、患肢压力及步态积分、血尿酸值、白细胞计数及肾脏重量系数。结果:痛风颗粒能有效抑制大鼠踝关节、足跖肿胀以及患肢压力和步态积分,并能显著改善高尿酸血症大鼠体内尿酸水平,高剂量痛风颗粒能明显抑制白细胞增生。结论:痛风颗粒具有抑制炎症及降低血清高尿酸的作用。     

槲皮素治疗大鼠急性痛风性关节炎的实验研究

目的观察槲皮素对尿酸钠致急性痛风性关节炎模型大鼠踝关节肿胀度的影响,并初步探讨其作用机制。方法采用大鼠右后肢踝关节腔内注射尿酸钠溶液制备急性痛风性关节炎模型,缚线法测定大鼠不同时相踝关节肿胀度,比色法测定大鼠血清、肝脏、脾脏和滑膜中MDA和NO含量以及SOD、GSH-PX、CAT等活性。结果槲皮素能够显著抑制痛风性关节炎大鼠踝关节肿胀度,降低NO和MDA水平,提高组织中SOD、CAT和GSH-PX活性。结论槲皮素具有抗痛风性关节炎作用,其作用与抗炎和抗氧化作用有关。     

双黄痛风胶囊抗痛风性关节炎作用研究

目的:研究双黄痛风胶囊(SHTF)抗痛风性关节炎的作用。方法:采用尿酸钠(MSU)建立大鼠及家兔痛风性关节炎模型,测定大鼠足肿胀程度,家兔关节滑膜液量、滑膜液中白细胞数及关节滑膜组织炎症病变程度,观察SHTF抗痛风性关节炎作用。结果:大鼠灌胃SHTF5、10、20g.kg-1,能显著减轻其足肿胀程度;家兔口服SHTF4、8、16g.kg-1,能显著减少其痛风性关节滑膜液量和滑膜液中白细胞数;家兔口服SHTF8、16g.kg-1,能显著减轻其关节滑膜组织炎症病变程度。结论:SHTF对MSU所致痛风性关节炎具有显著的保护作用。     

Difficult-to-treat gouty arthritis: a disease warranting better management

Gouty arthritis is the most common inflammatory arthritis in adults and is characterized by very painful flares. Gouty arthritis results from an elevated body uric acid pool, which leads to deposition of monosodium urate crystals, mainly in the joints. These crystals trigger the release of proinflammatory cytokines, in particular interleukin (IL)-1β, which stimulates inflammation. Gouty arthritis can progress to a chronic, deforming and physically disabling disease through the development of disfiguring tophi, joint destruction and persistent pain. Standard treatments are effective in most patients. Acutely, anti-inflammatory therapies provide rapid pain relief and resolution of flares. Chronically, urate-lowering therapies reduce serum urate levels and, in combination with anti-inflammatory prophylaxis, reduce the risk of flares. However, for a growing number of patients, current standard treatments are ineffective or are contraindicated, largely due to the presence of co-morbidities. Indeed, metabolic syndrome, hypertension, dyslipidaemia, cardiovascular disease, diabetes mellitus and renal impairment are all highly prevalent in individuals with gouty arthritis, and may lead to standard treatments being ineffective or inappropriate. Such patients with difficult-to-treat disease require alternative therapies. Gouty arthritis can have a major impact on health-related quality of life (HR-QOL), especially in patients with difficult-to-treat disease, as revealed by recent studies comparing HR-QOL for patients with gouty arthritis with that of the general population. All studies revealed clinically significant reductions in physical functioning for individuals with gouty arthritis compared with the general population. The difference was particularly marked for patients with difficult-to-treat disease. Gouty arthritis also constitutes an important economic burden through absence from work and medical costs. Again, the burden is greater in patients with difficult-to-treat disease. The development of difficult-to-treat disease reflects the short-comings of current standard treatments in a growing number of gouty arthritis patients. This has been recognized by the pharmaceutical industry and has promoted the development of innovative therapies. An appreciation of the key role of IL-1β in inflammation in gouty arthritis has led to the development of a new class of anti-inflammatory agents that block IL-1β signal transduction. The current IL-1β blockers in trials are rilonacept and canakinumab. Canakinumab, a fully human anti-IL-1β monoclonal antibody, has been shown to produce rapid and sustained pain relief from acute flares in patients with difficult-to-treat disease, and both rilonacept and canakinumab have been shown to reduce the risk of recurrent flares. Promising new therapies for reducing serum urate levels are also being developed. These include the recently approved therapies pegloticase (a pegylated form of the enzyme uricase that converts urate to allantoin), inhibitors of renal urate transporter proteins, and inhibitors of purine nucleotide phosphorylase, an enzyme involved in purine metabolism. Further studies are warranted to establish the value and role of these new therapies in the management of gouty arthritis. These new options should help reduce the growing human burden associated with gouty arthritis, lowering the tophaceous burden, minimizing the risk of flares, and enabling patients to achieve rapid and effective pain relief when flares do occur.     

复方水牛角提取物镇痛、抗炎作用的实验研究

目的:研究复方水牛角水提取物和醇提取物对尿酸钠所致大鼠急性痛风性关节炎(AGA)、冰醋酸致小鼠疼痛及二甲苯致小鼠耳壳炎症的作用.方法:采用2.5%尿酸钠溶液造成大鼠AGA模型,以0.6%冰醋酸溶液致小鼠疼痛扭体模型,以二甲苯造成小鼠耳壳急性炎症模型.分别以大鼠的踝关节肿胀度、血清尿酸含量,小鼠的扭体次数和耳廓肿胀度为指标,测定复方水牛角水提取物和醇提取物的镇痛、抗炎活性.结果:复方水牛角水提取物和醇提取物对尿酸钠所致AGA大鼠踝关节肿胀有明显抑制作用,在造模24 h时模型对照组关节肿胀率为(64.49±9.48)%,复方水牛角水提取物和醇提取物高剂量组关节肿胀率分别为(41.95±11.18)%和(42.32±6.85)%(P＜0.01),并能明显降低血尿酸水平.复方水牛角水提取物和醇提取物可减少冰醋酸所致小鼠扭体次数,减轻二甲苯所致小鼠耳廓肿胀程度.结论:复方水牛角提取物具有镇痛、抗炎作用,其机制可能与降低血清中尿酸水平有关.     

Astragaloside IV possesses antiarthritic effect by preventing interleukin 1β-induced joint inflammation and cartilage damage

The saponin astragaloside IV (AST) is one of major active components purified from Astragalus membranaceus (Fisch) Bge, which has been used in traditional Chinese medicine to treat immune disorders including rheumatoid arthritis (RA). The effects of AST on the suppression of experimental arthritis and its possible mechanisms are unknown. We measured the paw swelling of ankle joints, splenocyte proliferation, interleukin 1β (IL-1β), tumor necrosis factor α (TNFα) and nitric oxide (NO) formation by macrophages in rat adjuvant-induced arthritis (AIA). Intraarticular injection of IL-1β to rat knee joint for inducing the edema and in vitro IL-1β-stimulated cartilage impairment were examined. The results showed that oral treatment of AST (100 mg/kg/day) suppressed the joint inflammation and inhibited IL-1β, TNFα and NO production in macrophages from AIA rats. Macrophages were one of AST targeted cells, and mediated the reduced splenocyte proliferation in AIA rats. In addition, AST reduced the swelling induced by intraarticular injection of IL-1β, and protected against IL-1β-induced damage of cartilage proteoglycan synthesis and chondrocyte proliferation. We conclude that AST possesses antiarthritic effect and prevents IL-1β-induced joint inflammation and cartilage destruction. These findings suggest that AST may be used for the treatment of RA and other inflammatory joint diseases.     

甲氨蝶呤对炎性细胞因子及丝裂原活化蛋白激酶信号通路的影响

目的：探讨甲氨蝶呤（methotrexate,MTX）对类风湿关节炎（RA）发病起重要作用的炎性细胞因子IL-1β和TNF-α的作用及其可能的机制.方法：用Ⅱ型胶原建立类风湿关节炎（CIA）动物模型,以MTX（0.2 mg/kg/W）进行处理,6周后处死大鼠,取血清进行IL-1β和TNF-α检测;分离大鼠膝关节取关节滑膜细胞（FLS）进行培养、鉴定,检测脂多糖（LPS）诱导的FLS培养上清中IL-1β和TNF-α的含量,并观察MTX对FLS分泌IL-1β和TNF-α的影响;在FLS的培养中加入不同剂量的MTX,用Westen Blot方法检测FLS中ERK蛋白及磷酸化蛋白的表达.结果：关节炎指数评分、关节肿胀度测定及关节病理显示造模成功,分离关节滑膜细胞经流式细胞仪检测FLS的血管细胞黏附分子-1（VCAM-1）的表达为85.5％.造模后,CIA大鼠血清IL-1β和TNF-α明显增加,与空白对照组比较有统计学差异（P＜0.05）,MTX能有效减少CIA大鼠血清中IL-1β和TNF-α的含量（P＜0.05）,但未能恢复至正常水平.MTX能抑制LPS诱导的CIA大鼠关节FLS分泌IL-1β和TNF-α.Western Blot检测显示,不同浓度的MTX对CIA大鼠FLS中ERK蛋白的表达与模型对照组相比无统计学差异（P＞0.05）.CIA大鼠FLS中p-ERK蛋白的表达明显高于空白对照组（P＜0.01）,MTX干预后,低剂量组对p-ERK蛋白表达无明显影响,而中、高剂量组可降低p-ERK蛋白的表达（P＜0.05）.结论：MTX既有免疫抑制作用,同时还通过抑制炎性细胞因子IL-1β和TNF-α而具有抗炎作用,其机制可能部分与其抑制MAPK信号通路中的ERK蛋白磷酸化有关.     

健力舒纯粉对佐剂性关节炎模型大鼠肿瘤坏死因子-α释放的影响研究

目的:研究健力舒纯粉对佐剂性关节炎大鼠肿瘤坏死因子-α(TNF-α)释放的影响。方法:采用大鼠足跖注射Freundi's完全佐剂形成佐剂性关节炎(AIA),观察健力舒纯粉对模型大鼠超敏反应、炎症左右足跖厚度差异及血清TNF-α、白细胞介素-2(IL-2)和循环免疫复合物(CIC)的含量变化。结果:模型大鼠右后跖从第2天开始肿胀持续15d(原发性损害),健力舒纯粉可依赖性抑制模型大鼠足肿胀的程度,抑制TNF-α、IL-2的释放和降低CIC含量而发挥抗炎作用。结论:健力舒纯粉具有抗AIA、降低致炎因子及相关炎症介质的作用。