黄芩苷对尿酸钠诱导RAW264.7细胞NLRP3及炎症因子表达的影响

摘要

Objective:To explore the antigout mechanism of baicalin by investigating its effects on the expression of NLRP3 inflammatory and some inflammatory factors in monosodium urate-induced RAW264.7 macrophages.Methods:Cultured murine RAW264.7 macrophages in vitro were divided into control group,experimental drug groups which pre-received different concentrations of baicalin at final concentration of 2.5,5,10 or 20 μg· mL-1,respectively for 1 h before being induced by monosodium urate suspension at final concentration of 2 mg· mL-1,and model group which was treated by monosodium urate suspension at final concentration of 2 mg· mL-1.Twenty-four hours later the cells were collected and the mRNA expression of TNF-α,IL-1β,IL-18 and NLRP3 was determined by fluorescence quantitative PCR method and the levels of TNF-α,IL-1β and IL-18 in cell supernatant were detected by ELISA.Results:Compared with the control group,the gene expression of NLRP3,TNF-α,IL-1 β and IL-18 was significantly upregulated and the levels of TNF-α,IL-1 β and IL-18 were significantly increased by monosodium urate in the model group,and compared with the model group,the gene expression of TNF-α,IL-1β,IL-18 and NLRP3 and their contents were significantly inhibited in the baicalin-treated groups.Conclusion:Monosodium urate activates NLRP3 inflammasome and facilitates the excretion of TNF-α,IL-1 β and IL-18,and baicalin can significantly inhibit the phenomenon and has anti-inflammatory effect.%目的:研究黄芩苷对尿酸钠诱导RAW264.7细胞NLRP3炎性小体及炎症因子表达的影响.方法:取RAW264.7细胞分为对照组、模型组和药物组,模型组用尿酸钠(终浓度2 mg·mL-1)刺激,药物组先加入不同浓度黄芩苷(终浓度为2.5,5,10和20μg·mL-1)预处理1h后再加入尿酸钠.24 h后收集细胞,用qRT-PCR法检测TNF-α,IL-1β,IL-18和NLRP3的mRNA表达水平;收集细胞培养上清液,用ELISA法检测TNF-α,IL-1β和IL-18的浓度.结果:与对照组比较,模型组巨噬细胞NLRP3及炎症因子TNF-α,IL-1β和IL-18的基因表达显著上调,巨噬细胞分泌TNF-α,IL-1β和IL-18显著增加;与模型组比较,黄芩苷组显著抑制上述指标.结论:NLRP3炎性小体参与尿酸钠诱导的炎性反应,黄芩苷可抑制NLRP3的mRNA表达,减少炎症因子TNF-α,IL-1β和IL-18的分泌而发挥抗炎作用.