摘要
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·m L^(-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·m L^(-1))预处理1 h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。
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-I , 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 2mg·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-1 β and IL-18 in cell supernatant were detected by ELISA. Results: Compared with the control group, the gene expression of NLRP3, TNF-α, IL-11βand IL-18 was significantly upregulated and the levels of TNF-α, IL-1β 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-1β and IL-18, and baicalin can significantly inhibit the phenomenon and has anti-inflammatory effect.
出处
《中国新药杂志》
CAS
CSCD
北大核心
2018年第2期190-194,共5页
Chinese Journal of New Drugs