芹菜素通过NF-κB和MAPK抑制脂多糖诱导的骨髓来源巨噬细胞的炎性

Inhibition of apigenin on lipopolysaccharide-induced bone-marrow-derived macrophages inflammation through NF-κB and MAPK

中文关键词:  芹菜素  骨髓来源的巨噬细胞  脂多糖  NF-κB  MAPK

英文关键词:apigenin  bone-marrow-derived macrophages  lipopolysaccharide  NF-κB  MAPK

中文摘要:

      目的 研究芹菜素在脂多糖(lipopolysaccharide, LPS)诱导的骨髓来源巨噬细胞(bone-marrow- derived macrophages, BMDMs)炎性的作用。方法 用MTT方法筛选出芹菜素起作用的浓度范围。选择适当的芹菜素浓度处理BMDMs, 用实时定量PCR方法检测炎性基因的表达, 用Western-blot方法检测炎性信号通路蛋白的表达, 以及荧光免疫检验法考察NF-κB P65蛋白的核转位。结果 芹菜素的有效作用浓度范围为0~30 μmol/L, 选用10、30 μmol/L浓度的芹菜素培养BMDMs后, 炎性因子的mRNA水平明显降低, 巨噬细胞从促炎性M1型向抗炎性M2型转化, 并且呈现剂量依赖的趋势。NF-κB和MAPK信号通路的激活也受到了明显的抑制。结论 芹菜素能通过抑制NF-κB和MAPK信号通路降低LPS诱导的BMDMs的炎性。

英文摘要:

      Objective To investigate the effect of apigenin on lipopolysaccharide (LPS) induced inflammation and in bone-marrow-derived macrophages (BMDMs). Methods The apigenin dosage range that did not influence cell viability was detected by MTT assay. After choosing the suitable dose of apigenin to co-culture with BMDMs, the inflammatory genes expression was detected by RT-PCR, proteins expression which participated in inflammatory signaling pathways was detected by Wstern-blot, and NF-κB P65 nuclear translocation was investigated by immunofluorescence. Results The effective dose of apigenin was between 0~30 μmol/L. By choosing 10 and 30 μmol/L apigenin to co-culture with BMDMs, inflammatory cytokines were reduced in mRNA level, BMDMs transformed from M1 inflammatory macrophages to anti-inflammatory M2 macrophages and all these results showed in a dose-dependent manner. Apigenin also inhibited NF-κB and MAPK signaling pathways significantly. Conclusion Apigenin can reduce LPS-induced macrophages inflammation and partly through NF-κB and MAPK signaling pathways.