雷公藤甲素配伍甘草酸对CIA大鼠血清TNF-α,IL-10的影响

目的:观察雷公藤甲素与甘草酸配伍对CIA模型大鼠关节肿胀和血清TNF-α,IL-10水平的影响.方法:使用Ⅱ型胶原诱导出成功的关节炎模型大鼠60只,并随机分为模型组、雷公藤甲素组、甘草酸组、雷草1组、雷草2组和雷草3组,另设空白组.以关节炎指数和关节肿胀度作为疗效评判标准,并采用ELISA方法检测大鼠血清中抗Ⅱ型胶原抗体,TNF-α和IL-10的水平.结果:经雷公藤甲素配伍甘草酸治疗后,模型大鼠的关节炎指数和关节肿胀度均显著下降(P＜0.01),血清中抗Ⅱ型胶原抗体和TNF-α水平显著下降,而IL-10水平显著升高(P＜0.05,P＜0.01).结论:甘草酸配伍雷公藤甲素治疗CIA,可以在保持疗效的前提下减少雷公藤甲素的用量.     

蒙药忠伦阿汤对胶原诱导性关节炎大鼠血清炎性细胞因子的影响

目的 探讨蒙药忠伦阿汤对类风湿关节炎(RA)模型大鼠抗Ⅱ型胶原(CⅡ)抗体及白细胞介素1(IL-1)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)炎性细胞因子的影响.方法 取Wistar大鼠80只,随机选取68只造模,其余12只作为空白组,以牛Ⅱ型胶原皮下注射诱导建立胶原诱导性关节炎(CIA)大鼠模型,再将造模成功的62只大鼠随机分为模型组及忠伦阿汤低、中、高剂量组和雷公藤组各12只,剩余大鼠剔除.忠伦阿汤低、中、高剂量组分别予忠伦阿汤0.35g/kg、0.7g/kg、1.5g/kg,雷公藤组予雷公藤多苷片5mg/kg,空白组和模型组给予等体积生理盐水,各组灌胃给药6周后,采用酶联免疫吸附法(ELISA)测定抗CⅡ抗体、IL-1、IL-6、TNF-α的水平.结果 与空白组比较,模型组血清中抗CⅡ抗体、IL-1、IL-6、TNF-α含量均明显升高(P＜0.01),各药物组均可降低血清抗CⅡ抗体及炎性细胞因子的含量,忠伦阿汤中剂量组、高剂量组与雷公藤组在降低IL-1、IL-6、TNF-α水平方面差异无统计学意义(P＞0.05).结论 蒙药忠伦阿汤可能通过调节免疫,降低血清IL-1、IL-6及TNF-α的含量,减轻炎性细胞因子对关节炎的刺激作用,发挥干预类风湿关节炎的作用.     

白花蛇舌草治疗大鼠胶原诱导性关节炎的实验研究

目的探讨白花蛇舌草(HD)对胶原诱导性关节炎(CIA)大鼠模型的抗炎效果及其免疫学机制。方法首先建立Wistar大鼠CIA模型,造模成功后随机分为正常对照组、CIA模型对照组、白花蛇舌草正常量组、白花蛇舌草高剂量组、雷公藤组并给予相应处理。每周观察各给药组的关节炎指数,于第6周处死大鼠检测各组血清的TNF-α、IL-6的水平。结果 HD组大鼠关节炎指数显著降低(P<0.05或0.01);免疫后第6周,2个HD组大鼠血清TNF-α及IL-6的水平较CIA模型组明显降低(P<0.05),与雷公藤组当。结论 HD能够缓解CIA大鼠症状、控制炎症,其机制是抑制TNF-α和IL-6的水平。     

蓬草除痹汤对类风湿关节炎免疫调节作用的实验研究

目的观察蓬草除痹汤(PCCB)对Ⅱ型胶原诱导关节炎(CIA)大鼠模型外周血中细胞因子IL-17、IL-1β、TNF-α及T细胞亚群CD4+T、CD8+T、CD4+T/CD8+T的干预作用,探讨PCCB治疗类风湿关节炎(RA)的抗炎免疫作用机制。方法建立CIA大鼠模型,随机分为PCCB组、雷公藤组、空白组及模型组,连续给药28 d,采用酶联免疫吸附(ELISA)法、流式细胞术评价PCCB对CIA大鼠关节炎指数(AI)及大鼠血清IL-17、IL-1β、TNF-α和CD4+T、CD8+T、CD4+T/CD8+T表达的影响。结果治疗28 d后,PCCB组、雷公藤组关节肿胀度及AI显著改善(P均0.01);血清IL-17、IL-1β、TNF-α水平明显降低(P均0.01);CD4+T降低,CD8+T升高,CD4+T/CD8+T显著降低,且PCCB组的抑制作用明显优于雷公藤组(P0.05)。结论 PCCB能有效改善CIA大鼠关节炎指数,下调大鼠血清中致炎因子IL-17、IL-1β、TNF-α的水平,调节大鼠血清中CD4+T、CD8+T及CD4+T/CD8+T比例,这可能是PCCB治疗RA的主要机制,为临床应用及进一步研究奠定了基础。     

蓬草除痹汤对Ⅱ型胶原蛋白诱导性关节炎大鼠血清IL-1β、TNF-α及PGE2影响的实验研究

目的：观察蓬草除痹汤对Ⅱ型胶原蛋白诱导关节炎（CIA）大鼠血清IL—1β、TNF—α及PGE2的影响及作用机制。方法：建立Ⅱ型胶原蛋白诱导大鼠类风湿性关节炎模型,随机分为蓬草除痹汤高、中、低剂量纽、雷公藤组及空白组,观察6周,评价蓬草除痹汤对CIA大鼠右足踝关节肿胀度的抑制作用,对体重及外周血清1L-1βα、TNF-α及PGE2水平的影响。结果：与模型组比较,各用药组可显著抑制大鼠右足踝关节肿胀的程度（P〈0．01,P〈0．05）;蓬草除痹汤中、高剂量组均可明显提高大鼠体重增加速度（P〈0．01,P〈0．05）;各用药纽改善血清IL-1β、TNF—α及PGE2水平均明显优于模型组（P〈0．01）,其中蓬草除痹汤中、高剂量组的抑制作用明显优于雷公藤多甙片组（P〈0．05）。结论：蓬草除痹汤能有效改善CIA大鼠关节炎症状,其机制可能与下调血清中致炎因子IL-1β、TNF—α及PGE2的水平有关,值得进一步开发研究。     

清痹颗粒对关节炎模型大鼠免疫因子的影响

目的:观察清痹颗粒对大鼠Ⅱ型胶原性关节炎(CIA)相关免疫学指标的影响。方法:用Ⅱ型胶原(CⅡ)诱导大鼠胶原性关节炎(CIA)模型,给药后,检测血清中CⅡ抗体、TNF-α,组织中IL-2水平,脾细胞中TNF-α。结果:清痹颗粒显著降低关节周围组织的IL-2水平,显著降低CⅡ抗体水平,降低TNF-α水平。结论:清痹颗粒对Ⅱ型胶原性关节炎模型大鼠免疫因子有明显的改善作用。     

清络通痹方与精简方的药效学比较

目的:探讨清络通痹方精简前后的药效学作用及影响机制。方法:DBA/1小鼠,复制胶原性关节炎(CIA)模型,随机分为空白组,模型组,清络通痹精简方组(8.4 g·kg-1),清络通痹原方组(13 g·kg-1)及雷公藤多苷片组(9 mg·kg-1),观察一般情况及关节肿胀,ig给药4周后,检测血清中白介素-1β(IL-1β),肿瘤坏死因子-α(TNF-α),抗Ⅱ型胶原抗体(抗CⅡ抗体)含量;踝关节HE染色观察病理学改变及病理评分。结果:与正常组比较,模型组小鼠关节肿胀明显,关节炎评分,TNF-α,IL-1β和抗CⅡ抗体水平明显升高(P0.01);与模型组比较,清络通痹精简方及原方、雷公藤多苷均能明显抑制小鼠足肿胀,降低关节炎评分,降低血清中TNF-α,IL-1β和抗CⅡ抗体水平(P0.01,P0.05);病理学检查提示可减轻关节病理损伤,关节总病理评分降低(P0.01)。结论:清络通痹精简方将不同性味、不同功效药物合理配伍,治疗效果和作用机制与原方相似。     

雷公藤多苷片对胶原诱导性关节炎大鼠血清HMGB1和IL-17的影响

目的:观察雷公藤多苷片对胶原诱导性关节炎(collagen induced arthritis,CIA)大鼠血清中高迁移率族蛋白B1(high mobility group box chromosomal protein 1,HMGB1)及白介素17(interleukin 17,IL-17)含量的影响.方法:40只SD大鼠被随机分为正常对照组、模型对照组、甲氨喋呤对照组(3 mg·kg-1)、雷公藤多苷片低、高剂量组(5,10 mg·kg-1).用牛Ⅱ型胶原蛋白加不完全氟氏佐剂诱导大鼠关节炎模型,于免疫12d开始灌胃给药,连续4周.CIA大鼠模型建立后,观察各组大鼠关节指数变化,并采用ELISA法检测各组大鼠血清中HMGB1和IL-17的含量.结果:与正常组比较,模型组大鼠关节肿胀明显,血清中HMGB1和IL-17含量明显升高(P＜0.01或P＜0.05);与模型组比较,各治疗组大鼠关节肿胀程度均有一定程度缓解,甲氨喋呤组和雷公藤多苷片高剂量组大鼠血清中HMGB1和IL-17的含量显著低于模型组(P＜0.01或P＜0.05).结论:雷公藤多苷片治疗CIA大鼠关节肿胀可能与降低血清中HMGB1,IL-17的含量相关.     

姜酚对胶原诱导性关节炎的抗炎作用及其机制研究

目的探讨姜酚对牛II型胶原诱导性关节炎(Collagen Induced Arthritis,CIA)大鼠的抗炎作用及其机制。方法将6周龄雌性Wistar大鼠随机分为空白对照组、模型组、姜酚组和雷公藤多苷组,每组10只。制备CIA模型,观察姜酚对CIA大鼠关节病理、关节炎指数的变化及对大鼠血清肿瘤坏死因子-α(TNF-α)、白介素-1(IL-1)、白介素-1β(IL-1β)表达的影响。结果姜酚能够抑制CIA大鼠踝关节肿胀,降低关节炎指数,并能降低血清TNF-α、IL-1及IL-1β水平,减轻关节滑膜细胞增生、滑膜层及滑膜下层淋巴细胞浸润,其疗效与雷公藤多苷组相当(P>0.05)。结论姜酚对CIA大鼠关节炎具有治疗作用,其机制可能与下调TNF-α、IL-1和IL-1β有关。     

蕲蛇水提取物对胶原诱导性关节炎大鼠血清TNF-α、IL-6和IL-10的影响

目的:探讨蕲蛇水提取物对胶原诱导性关节炎(CIA)大鼠血清中肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)和白介素-10(IL-10)的影响。方法:大鼠随机分为正常对照组,CIA模型组,蕲蛇水提取物高、中、低剂量组,醋酸泼尼松组(PAT)。用牛Ⅱ型胶原诱导大鼠CIA模型。治疗过程中观察大鼠的关节肿胀程度、关节炎指数。治疗21d后处死大鼠,采用ELISA方法观察大鼠血清中的TNF-α、IL-6和IL-10的水平。结果:给药后治疗组能降低大鼠的踝关节肿胀程度,关节炎指数及大鼠血清TNF-α,升高血清中IL-10。结论:蕲蛇可以显著减轻CIA大鼠踝关节肿胀程度和关节炎指数,并且呈剂量—效应相关。蕲蛇水提取物高剂量组可以抑制CIA大鼠异常的自身免疫反应,通过下调血清中TNF-α含量,上调IL-10的含量,调节其免疫状态,达到治疗CIA的作用。     

京尼平苷对类风湿性关节炎大鼠血清IL-1β和TNF-α的影响

目的:研究京尼平苷对类风湿性关节炎大鼠血清IL1β和TNFα的影响,进一步探讨该药物的作用机制。方法:建立Ⅱ型胶原蛋白诱导大鼠类风湿性关节炎模型。观察京尼平苷对实验性大鼠足肿胀的抑制作用;检测血清IL1β和TNFα的水平。结果:与模型组比较,京尼平苷可以延缓对侧肢体足肿胀发生的时间,抑制大鼠足肿胀的程度(P<0.01);用药后,中、高剂量给药组血清IL1β和TNFα水平明显低于模型组(P<0.01)。结论:京尼平苷在类风湿性关节炎大鼠中可以下调致炎因子IL1β和TNFα的水平,提示这可能与该药抑制实验性类风湿性关节炎病情进展密切相关。     

Preliminary study of effects and mechanisms of Qingpeng paste on type II collagen-induced arthritis in rats

OBJECTIVE: To investigate the effect of Qingpeng paste (QP) on collagen-induced arthritis (CIA) in rats. METHOD: CIA was established in female Wistar rats with injection of type II bovine collagen at the base of the tail of animals. CIA rats were treated daily with external administration of different doses of QP or voltaren beginning on the day after the onset of arthritis (day 1) until day 20. Paw swelling rate and the serum levels of IL-1 beta were determined. Moreover, the expression of TNF-alpha and IL-alpha and histopathological changes in the arthritic joints were also observed. RESULT: QP markedly suppressed the paw swelling rate of arthritic rat, reduced the expression of TNF-alpha and IL-alpha in synovial membrane. Histopathological changes in the arthritic joints were also significantly ameliorated in the QP-treated versus vehicle-treated rats. However, the elevated serum levels of IL-1 beta in arthritic rats were not influenced by QP. CONCLUSION: The present findings demonstrate the protective property of QP on collagen-induced arthritis, mechanisms underlying it may be related to reduce the expression of IL-1alpha and TNF-alpha in synovial membrane.     

Anti-inflammatory effect of bee venom on type II collagen-induced arthritis

Bee venom (BV) has been used to relieve pain and reduce inflammation in traditional Oriental medicine, especially in chronic inflammatory diseases such as rheumatoid arthritis (RA). We previously reported that the BV injection into a traditional acupuncture point (Zusanli) reduced arthritis-associated edema and nociceptive responses in Freund's adjuvant-induced arthritis in rats (Kwon et al., 2001). This study was designed to evaluate the anti-inflammatory and anti-cytokine effect of BV on a murine type-II collagen-induced arthritis (CIA) model. Male mice were immunized by spontaneous injection of 100 microg of an emulsion of bovine type-II collagen and complete Freund's adjuvant (CFA), with a booster injection after 2 weeks. In the experimental group, 0.1 ml BV was injected at acupuncture point (Zusanli) near both knees twice a week for a total of 5 times. In the control group, normal saline was injected at the same frequencies. These injections began 5 weeks after the first collagen injection. Starting the 3rd week after the first collagen injection, we examined limb swelling and severity of arthritis twice a week. At 8 weeks, mice were sacrificed and synovial tissue was examined with the light microscope and serum cytokines (IL-1beta and TNF-alpha) were measured by ELISA. The incidence of arthritis, the mean arthritis index and the number of arthritic limbs were significantly lower in the treatment compared to the control group (63% versus 75%, 3.4% versus 8.5%, 23% versus 75%, respectively). Among the serum proinflammatory cytokines, the production of TNF-alpha in the BV group was suppressed compared to the control group (59 +/- 4.5 versus 99.5 +/- 6.5, p < 0.05), but IL-1beta was not suppressed. The examination of the histopathology of the joints of murine CIA showed decreased inflammation signs and less lymphocyte infiltration after BV acupuncture therapy. Acupuncture therapy with BV suppressed the development of arthritis and caused inhibition of the immune responses in type-II collagen-induced arthritis.     

竹节三七总皂苷对胶原诱导型关节炎大鼠抗氧化能力、细胞因子水平的影响

目的:研究竹节三七总皂苷(total saponins of Panax japonicus,TSPJ)对胶原诱导型关节炎大鼠抗炎、抗氧化功能的影响。方法:注射Ⅱ型胶原蛋白与完全费氏佐剂的乳化剂建立大鼠关节炎模型。观察致炎前后大鼠足容积的改变检测竹节三七总皂苷对关节炎模型大鼠的作用效果。检测关节炎大鼠抗氧化指标及血清细胞因子水平,观察竹节三七总皂苷对模型大鼠抗炎作用机理。结果:与模型组比较,25 mg/kg、50 mg/kg、100 mg/kg竹节三七总皂苷能减轻关节炎大鼠足爪肿胀度,100mg/kg组尤为明显;100mg/kg竹节三七总皂苷增加模型大鼠血中谷胱甘肽过氧化物酶、超氧化物歧化酶活性,抑制丙二醛水平;100mg/kg竹节三七总皂苷能降低模型大鼠血中白细胞介素-1、白细胞介素-8、肿瘤坏死因子-α水平,50mg/kg竹节三七总皂苷低模型大鼠血中白细胞介素-8水平效果明显。结论:竹节三七总皂苷具有抗炎作用,能增强关节炎大鼠的抗氧化能力,降低关节炎大鼠白细胞介素-1、白细胞介素-8、肿瘤坏死因子-α水平,可能是其治疗类风湿性关节炎的重要机制之一。     

Suppression of the onset and progression of collagen-induced arthritis in rats by QFGJS, a preparation from an anti-arthritic Chinese herbal formula

QFGJS is an herbal preparation, and its pronounced effectiveness in treating adjuvant-induced arthritis (AIA) has been previously demonstrated. We herein aimed to confirm its anti-arthritic effect on collagen-induced arthritis (CIA) in rats. CIA was established in female Wistar rats with intradermal injection of type II bovine collagen at the base of the tail of animals. CIA rats were treated daily with oral administration of different doses of QFGJS beginning on the day of the induction of arthritis (day 0, the prophylactic treatment) or on the day after the onset of arthritis (day 13, the therapeutic treatment) until day 30. The results showed that prophylactic treatment with QFGJS significantly suppressed the onset of arthritis, and therapeutic treatment with QFGJS markedly reduced paw swelling and ESR levels even in the established CIA. Radiologic and histopathologic changes in the arthritic joints were also significantly reduced in the QFGJS-treated versus vehicle-treated rats. Moreover, the serum levels of pro-inflammatory cytokines TNF-alpha, IL-1beta, and IL-6 were markedly lowered in the QFGJS-treated rats. Hence, our studies demonstrate the quality, safety, and effectiveness of QFGJS as an anti-arthritic agent, which makes QFGJS a strong candidate for further clinical trials on rheumatoid arthritis (RA) patients.     

Suppressive effects of a water extract of Ulmus davidiana Planch (Ulmaceae) on collagen-induced arthritis in mice

Ulmus davidiana Planch (Ulmaceae) has long been known to have anti-inflammatory and protective effects on damaged tissue, inflammation and bone resorption. Therefore, this study was undertaken to address (1) whether the water extract of the bark of Ulmus davidiana Planch (Ulmaceae) (UD) can modulate the expression of inducible inflammatory cytokines in mice; (2) in order to assess the therapeutic effects of UD in collagen-induced arthritis (CIA) in mice. DBA/1 mice were immunized with bovine type II collagen. After a second collagen immunization, mice were treated with UD orally at 100mg/kg once a day for 3 weeks. Paws were evaluated macroscopically for redness, swelling and deformities. The levels of TNF-alpha and IL-1beta in the ankle were examined. The severity of arthritis within the knee joints was evaluated by histological assessment of cartilage destruction and pannus formation. Administration of UD significantly suppressed the progression of CIA and inhibited the production of TNF-alpha and IL-1beta in the paws. The erosion of cartilage was dramatically reduced in mouse knees after treatment with UD. In the serum of UD-treated mice, the levels of IL-4 and IL-10, anti-inflammatory cytokines, were increased. From the results, it was concluded that administration of UD has therapeutic effects on CIA including protection of cartilage and RA for a potential therapy.     

雷公藤多甙对大鼠胶原免疫性关节炎及佐剂性关节炎黏膜免疫功能影响的对比研究

目的观察雷公藤多甙对大鼠胶原免疫性关节炎（collagen-Ⅱ induced arthritis,CIA）及佐剂性关节炎（adjuvant arthritis,AA）黏膜免疫功能的影响。方法分别以Ⅱ型胶原加完全弗氏佐剂和完全弗氏佐剂单独致炎免疫大鼠造成CIA和AA模型,以雷公藤多甙治疗,观察大鼠黏膜、全身免疫指标（外周血T细胞亚群）以及关节局部炎症因子（IL-6、TNF—α、COX-2和NF-κB等）的变化。结果CIA模型组派伊尔结（Peyer’s patch,PP）CD4^＋、血中CD4^＋、CD8^＋均升高;AA模型组PPCD4^＋降低,CD8^＋升高,血中的CD4^＋,CD8^＋均升高。雷公藤对两模型组的PP和血中T细胞亚群存在不同影响。两种模型大鼠关节可见高水平IL-6、TNF—α、COX-2和NF—κB表达,雷公藤多甙可以抑制这些炎症介质的表达。结论两种关节炎模型在黏膜免疫反应方面及雷公藤多甙对这两种模型的影响存在异同。     

白芍总苷对大鼠胶原性关节炎及其免疫功能的影响

 目的研究白芍总苷(TGP)对大鼠胶原性关节炎(CIA)及其免疫功能的影响。方法采用鸡Ⅱ型胶原诱导大鼠CIA模型,关节评分法检测关节炎发生情况,ELSIA法检测大鼠血清中抗CⅡ抗体的水平,MTT法检测T细胞和B细胞增殖反应,IL-1、IL-2活性的测定采用小鼠淋巴细胞增殖法。结果大鼠于致炎后第14天开始出现多发性关节炎症状,体重减轻,血清中抗CⅡ抗体水平升高,TGPig给药,连续14d,能够明显抑制CIA大鼠的AI,促进大鼠体重的恢复,降低血清中抗CⅡ抗体水平。进一步研究表明,TGP体内、外给药均能抑制CIA大鼠增高的T、B淋巴细胞增殖反应,还能显著降低刀豆蛋白A(ConA)诱导的CIA大鼠脾淋巴细胞产生IL-2的能力以及脂多糖(LPS)诱导的腹腔巨噬细胞产生IL-1的能力。结论TGP对CIA大鼠具有治疗作用,其机制可能与其调节CIA大鼠异常的免疫功能,平衡细胞因子的产生有关。     

安宫牛黄散中朱砂、雄黄对外伤性脑水肿大鼠热休克蛋白、一氧化氮合酶和炎症细胞因子的影响

目的:探讨安宫牛黄散中朱砂、雄黄的药理作用机制。方法:SD大鼠随机分成6组(12只／组):正常对照组、外伤性脑水肿膜型对照组、朱砂组(0．15 g/kg)、雄黄组(0．15 g/kg)、安宫牛黄散(下简称整方)组(1．5 g/ kg)、去朱砂、雄黄的安宫牛黄散(下简称拆方)组(1．2 g/kg),以上各组再设8 h分组和24 h分组(6只／分组)。RT-PCR法测定脑组织中热休克蛋白70(HSP70)mRNA表达;比色法测定脑组织中一氧化氮合酶(NOS)及其同工酶(iNOS、cNOS)活力;放免法测定血清中细胞因子TNF-α、IL-1β水平。结果:造模后8 h,整方组与拆方组HSP 70 mRNA表达均较模型组增高(P<0．05),且整方组诱导HSP 70 mRNA表达的作用强于拆方组(P<0．05);朱砂、雄黄、整方和拆方均能降低iNOS活力,且较模型组明显降低(P<0．05),其中整方组抑制作用最为显著。雄黄组、整方组、拆方组TNF-α水平较模型组降低(P<0．05),整方组与拆方组IL-1β水平较模型组降低(P<0．05)。结论: HSP 70、iNOS、TNF-α及IL-β参与了外伤性脑水肿的病理过程。安宫牛黄散和复方中的朱砂、雄黄对外伤性脑水肿大鼠脑组织的保护作用可能与通过增加诱导HSP 70 mRNA表达、抑制iNOS活力和炎症细胞因子TNF-α、IL-1β的生成有关。     

Effects and mechanisms of total glucosides of paeony on synoviocytes activities in rat collagen-induced arthritis

The aim of the study was to investigate the effects of TGP, an active compound extracted from the roots of Paeonia lactiflora Pall, on the activities of synoviocytes in rats with collagen-induced arthritis (CIA) and its possible mechanisms. CIA was induced in male Sprague-Dawley (SD) rats immunized with chicken type II collagen (CII) in Freund's complete adjuvant (FCA). Synoviocytes proliferation was determined by 3-(4, 5-2dimethylthiazal-2yl) 2, 5-diphenyltetrazoliumbromide (MTT) assay. Tumor necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1), prostaglandin E(2) (PGE(2)) and cyclic adenosine monophosphate (cAMP) levels in synoviocytes were measured by radioimmunoassay (RIA). E-prostanoid (EP)(2) and EP(4) receptors were analyzed by Western blot analysis. The results showed that TGP significantly inhibited the proliferation of synoviocytes, decreased the production of IL-1, TNF-alpha and PGE(2) and elevated the levels of cAMP. Further study showed that TGP could up-regulate the expression of EP(2) and EP(4). These results indicated that TGP might exert its anti-inflammatory effects through inhibiting the production of pro-inflammatory mediators in synoviocytes of CIA rats, which might be associated with its ability to regulate cAMP-dependent EP(2)/EP(4)-mediated pathway.