论文部分内容阅读
【目的】观察黄芩苷对脂多糖(lipopolysaccharide,LPS)诱导的小鼠巨噬细胞CD36表达及炎症因子肿瘤坏死因子-α(TNF-α)分泌的影响。【方法】分别用LPS(终浓度0.1μg/mL)或LPS加黄芩苷(终浓度分别为50、100μmol/L)处理生长良好的小鼠巨噬细胞RAW264.7,采用实时荧光定量PCR法和流式细胞术检测黄芩苷对巨噬细胞CD36分子表达的影响,然后采用酶联免疫吸附(ELISA)法检测细胞上清液中TNF-α含量变化。【结果】LPS刺激可以诱导巨噬细胞CD36表达升高,与空白对照组比较差异有统计学意义(P<0.01);不同浓度黄芩苷预处理组可显著抑制LPS诱导的CD36基因转录和蛋白表达,与LPS组比较差异有统计学意义(P<0.01);黄芩苷还可显著减少巨噬细胞炎症因子TNF-α的分泌(P<0.05)。【结论】黄芩苷可通过抑制CD36表达,下调LPS诱导的巨噬细胞炎症因子TNF-α的生成从而发挥抗炎作用。
【Objective】 To observe the effect of baicalin on CD36 expression in macrophages induced by lipopolysaccharide (LPS) and the secretion of tumor necrosis factor-α (TNF-α). 【Methods】 Growth macrophages RAW264.7 cells were treated with LPS (final concentration 0.1μg / mL) or LPS plus baicalin (final concentration 50 and 100μmol / L), respectively. Real - time fluorescence quantitative PCR Flow cytometry was used to detect the effect of baicalin on CD36 expression in macrophages. The changes of TNF-α in supernatant were detected by enzyme-linked immunosorbent assay (ELISA). [Results] LPS stimulated the expression of CD36 in macrophages, which was significantly different from that of the blank control group (P <0.01). Different concentrations of baicalin pretreatment significantly inhibited the CD36 gene transcription and protein expression induced by LPS , Compared with LPS group, the difference was statistically significant (P <0.01). Baicalin also significantly reduced the secretion of inflammatory cytokines TNF-α (P <0.05). 【Conclusion】 Baicalin can exert anti-inflammatory effects by inhibiting the expression of CD36 and down-regulating LPS-induced macrophage inflammatory factor TNF-α production.