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通过建立大鼠佐剂性关节炎（ＡＡ）动物模型，研究了ＩＬ－１０和ＩＬ－１ｒａ对正常及ＡＡ大鼠腹腔Ｍφ分泌细胞因子的调节作用，并利用分子杂交技术在基因水平上对其作用机制进行了初步探讨。结果表明：ＡＡ大鼠腹腔Ｍφ呈高度活化状态，产生大量炎症细胞因子ＩＬ－１、ＩＬ－６、ＩＬ－８和ＴＮＦ等，ＩＬ－１０和ＩＬ－１ｒａ对正常及ＡＡ大鼠腹腔Ｍφ细胞因子的产生均呈显著抑制作用，并呈剂量依赖关系。ＩＬ－１０和ＩＬ－１ｒａ具有协同抑制作用。进一步研究发现ＩＬ－１０和ＩＬ－１ｒａ能抑制ＬＰＳ诱导的腹腔ＭφＩＬ－８ｍＲＮＡ表达，表明其抑制作用发生在基因水平上。提示ＩＬ－１０和ＩＬ－１ｒａ是有效的免疫抑制剂，从而为其临床抗炎应用提供了重要的理论和实验依据
Through the establishment of an animal model of adjuvant arthritis (AA) in rats, the regulatory effect of IL-10 and IL-1ra on Mφ-secreting cytokines in the peritoneal cavity of normal rats and AA rats was studied. The molecular hybridization Mechanism of action was discussed. The results showed that the Mφ of AA rats was highly activated and a large number of inflammatory cytokines IL-1, IL-6, IL-8 and TNF were produced in AA rats. IL-10 and IL- Were significantly inhibited, and in a dose-dependent manner. IL-10 and IL-1ra have a synergistic inhibitory effect. Further study found that IL-10 and IL-1ra can inhibit LPS-induced intraperitoneal MφIL-8mRNA expression, indicating that its inhibitory effect at the gene level. It is suggested that IL-10 and IL-1ra are potent immunosuppressive agents that provide important theoretical and experimental evidence for their clinical anti-inflammatory applications