目的观察脂氧素受体激动剂BML-111对大鼠佐剂诱导的关节炎(adjuvant arthritis,AA)病理改变及炎症因子表达的影响。方法6SD大鼠足跖部注射弗氏完全佐剂诱导建立AA动物模型,脂氧素受体激动剂BML-111于造模后每日腹腔注入。观察AA大鼠足爪肿胀情况并给予定量临床评分;取病变关节切片HE染色后,光学显微镜下观察关节组织病理改变;EILSA法检测血清中肿瘤坏死因子α(TNF-α)、白介素-6(IL-6)浓度。结果BML-111处理降低AA大鼠关节临床病变评分并减轻关节组织病理损伤,这一效应伴有血清中TNF-α和IL-6浓度明显降低。结论脂氧素受体激动剂BML-111可减轻佐剂诱导的大鼠关节病变,提示脂氧素可调节免疫介导的慢性炎症过程,在关节炎等慢性炎症性疾病中有潜在应用价值。
Aim To investigate the influence of lipoxin receptor agonist BML-111 on the histological changes and the production of pro-inflammatory cytokines in rats with adjuvant arthritis (AA). Methods AA was induced by intradermal injection of complete freund's adjuvant (CFA) into the left hind footpad of SD rats. The rats were then supplemented with BML-111 daily for 3 weeks. The swelling degree of hind paw was recorded and the clinical disease activity of AA was scored. At the end of the experiment, joint tissues were fixed and stained with HE routinely for morphologic evaluation, while the serum was collected for measuring the concentrations of TNF-α and IL-6 by ELISA. Results The swelling degree of hind paw and the clinical disease activity of AA was significantly decreased in BML-111-treated AA rats. Treatment of BML-111 attenuated the histopathological lesions of the joints. The concentrations of serum TNF-α and IL-6 were also decreased after BML-111 administration. Conclusions Lipoxin receptor agonist BML-111 alleviates CFA-induced adjuvant arthritis in rats. Lipoxin can also regulate chronic immune-mediated inflammatory process, implicating the potential pharmacological value of lipoxin in the clinical management of patients with chronic inflammatory diseases such as RA.