目的:建立小鼠佐剂性关节炎(AA)模型,研究资木瓜多糖(CSPS)对小鼠AA病理改变及炎症因子表达的影响。方法:雄性昆明鼠随机分为正常对照组、模型组、CSPS高、低剂量(分别为400,200 mg·kg-1)组、阳性药醋酸泼尼松(PAT,5.6mg·kg-1)组,每组10只。各组均于造模前1 d开始给药,2次/d,连续3 d;再于造模后第8天继续给药,2次/d,连续16 d。正常对照组、模型组ig等体积生理盐水。小鼠足部注射弗氏完全佐剂诱导建立AA动物模型,检测小鼠足爪的肿胀度,测定脾、胸腺、肝脏的指数,噻唑蓝(MTT)法检测脾淋巴细胞增殖反应,酶联免疫(ELISA)法检测脾细胞培养上清液中肿瘤坏死因子-α(TNF-α),白介素-1β(IL-1β),白介素-4(IL-4)的水平。结果:CSPS能有效减轻AA小鼠的原发性和继发性足肿胀,抑制免疫脏器指数的升高,抑制AA小鼠的脾淋巴细胞增殖反应,降低AA小鼠脾细胞TNF-α,IL-1β的产生,提高IL-4含量。结论:CSPS对AA具有抑制作用,其机制可能与抑制淋巴细胞增殖,减少促炎因子TNF-α,IL-1β释放,促进抗炎因子IL-4表达有关。 OBJECTIVE: To establish an animal model of adjuvant arthritis (AA) and study the effect of papaya polysaccharide (CSPS) on the pathological changes of AA and the expression of inflammatory cytokines in mice. Methods: Male Kunming mice were randomly divided into normal control group, model group, CSPS high and low dose groups (400 and 200 mg · kg -1, respectively) and positive group (PAT, 5.6 mg · kg -1) Each group of 10. Each group was administered 1 d before modeling, 2 times / d for 3 days, then on the 8th day after the model was continued, twice a day for 16 days. Normal control group, model group ig equal volume of saline. Mice were injected with complete Freund’s adjuvant to induce the establishment of AA animal models. The degree of swelling of the paws was measured. The indices of spleen, thymus and liver were measured. The proliferation of splenic lymphocytes was detected by MTT assay. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-4 (IL-4) in spleen cell culture supernatant were detected by ELISA. Results: CSPS could effectively reduce the primary and secondary foot swelling, inhibit the increase of immune organ index, inhibit the splenic lymphocyte proliferation reaction in AA mice and decrease the levels of TNF-α, IL-1β production, increase IL-4 content. CONCLUSION: CSPS has an inhibitory effect on AA, which may be related to the inhibition of lymphocyte proliferation, the release of proinflammatory cytokines TNF-α and IL-1β and the promotion of anti-inflammatory cytokine IL-4 expression.