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目的:观察石藤胶囊对大鼠佐剂性关节炎(adjuvant arthritis,AA)血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)含量的影响。方法:采用弗氏完全佐剂诱导的大鼠AA模型。选用Wistar大鼠,造模后第19天,将出现多发性关节炎症状的大鼠随机选取24只,并随机分为模型组、石藤胶囊组、雷公藤组,每组8只。注射生理盐水大鼠8只作为正常对照组。各组按每日10 mL·kg-1连续灌胃给药或给等体积生理盐水,持续21 d。其中石藤胶囊组每日灌服石藤胶囊0.75 g.kg-1,雷公藤组每日灌服雷公藤多苷片6 mg·kg-1,模型组和正常组灌服等体积的生理盐水。放射免疫法测定大鼠血清TNF-α,IL-1β,同时观察大鼠足爪肿胀抑制率、关节炎指数及关节病理积分的变化。结果:石藤胶囊可以明显降低AA大鼠血清TNF-α[模型组为(1.25±0.22)μg·L-1,石藤胶囊组为(0.88±0.11)μg·L-1,两组对比P<0.01]和IL-1β水平[模型组为(0.28±0.05)μg·L-1,石藤胶囊组为(0.20±0.03)μg·L-1,两组对比P<0.01)],降低AA大鼠的足爪肿胀度,提高对关节肿胀的抑制率。结论:石藤胶囊能够通过降低血清TNF-α和IL-1β水平对AA发挥治疗作用。
Objective: To observe the effects of Shi Teng capsule on serum levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in adjuvant arthritis (AA) rats. Methods: Rat AA model induced by complete Freund’s adjuvant was used. Wistar rats were selected. On the 19th day after model establishment, 24 rats with multiple arthritis symptoms were randomly selected and randomly divided into model group, ShiTu capsule group and tripterygium wilfordii group, with 8 rats in each group. Eight normal saline rats were injected as normal control group. Each group by 10 mL · kg-1 daily gavage or given an equal volume of saline for 21 days. The stone vine capsule was given a daily dose of 0.75 g.kg-1 and the tripterygium wilfordii tablet was given 6 mg · kg-1 of tripterygium wilfordii. The model group and the normal group were given the same volume of normal saline . The levels of TNF-α and IL-1β in serum of rats were measured by radioimmunoassay. At the same time, the changes of inhibition rate, arthritis index and pathological score of rat paw swelling were observed. Results: ShiTu capsule could significantly reduce serum TNF-α in AA rats [(1.25 ± 0.22) μg · L-1 in model group and (0.88 ± 0.11) μg · L-1 in Shiteng Capsule group, P < 0.01) and IL-1β level (0.28 ± 0.05) μg · L-1 in model group and (0.20 ± 0.03) μg · L-1 in Shiteng Capsule group, P <0.01) Rat paw swelling, improve the inhibition of joint swelling. Conclusion: ShiTu capsule can treat AA by decreasing serum levels of TNF-α and IL-1β.