目的 观察雷公藤次碱(wilforine)对脂多糖诱导的小鼠单核/巨噬细胞系RAW264.7细胞炎症模型中炎症因子的影响。方法 采用LPS刺激生长良好的RAW264.7细胞,建立细胞炎症模型。以CCK-8法检测不同浓度雷公藤次碱对RAW264.7细胞的毒性作用;以酶联免疫吸附试验检测细胞上清中肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)的含量;以硝酸还原酶法检测一氧化氮(NO)的含量。结果 雷公藤次碱在11.5-115 μmolL-1的浓度范围内,对RAW264.7细胞无毒性作用(p〉0.05);脂多糖可以明显诱导RAW264.7细胞分泌TNF-α、IL-6和NO(p〈0.01);雷公藤次碱可使TNF-α、IL-6和NO的释放受到抑制(p〈0.05,p〈0.01)。结论 雷公藤次碱可以抑制LPS诱导的RAW264.7细胞炎症反应,其抗炎作用与减少炎性细胞因子TNF-α、IL-6和NO的产生有关。
OBJECtIVE To investigate the effects of wilforine on the release of inflammatory cytokines from lipopolysaccha- ride-induced RAW 264. 7 cells. METHODS The inflammation model was constructed by treating RAW 264. 7 cells with lipopolysaccharide (LPS). The cytotoxieity of wilforine with different doses was examined by cell counting kit-8 (CCK-8) method; the levels of TNF-c~, IL-6 were tested by ELISA and NO was assayed by nitrate acid reductase method. RESULTS Wilforine showed no cytotoxicity on the growth of RAW 264. 7 cells at the concentrations from 11.5 to 115 9mol.L^-1 (P〉0. 05) ; LPS induced markedly increased secretions of TNF-α, IL-6 and NO from RAW 264. 7 cells; Meanwhile, wilforine significantly de- creased the levels of TNF-a, IL-6 and NO induced by LPS (P〈0. 05, P〈0. 01). CONCLUSION Wilforine has anti-inflammatory effect, which might be mediated by downregulation of the expression of inflammatory factors TNF-α, IL-6 and NO.