为检测游离脂肪酸对巨噬细胞解耦连蛋白2的影响,探讨肥胖与巨噬细胞解耦连的关系。采用培养RAW264.7巨噬细胞,分为空白对照组(基础培养液)、FFA组(基础培养液中加入FFA,终浓度为100μmol/L)和京尼平组(基础培养液中加入京尼平,终浓度为10μmol/L)。用Westernblot的方法检测药物干预后UCP2与NF-κB磷酸化的表达水平。结果显示,与空白对照组相比,FFA作用于巨噬细胞24h后细胞内UCP2与NF—κB磷酸化水平均升高,差异有统计学意义(P〈0.05);而京尼平作用于巨噬细胞24h后细胞内UCP2与NF-κB磷酸化水平均降低,差异有统计学意义(P〈0.05)。由此可知,FFA能诱导巨噬细胞的线粒体发生解耦连,NF—κB磷酸化水平升高。
To detect the effect of fatty acid on macrophages uncoupling protein 2 so as to explore the relationship between obesity and macrophages uncoupling. RAW264.7 macrophages were cultivated and divided into blank control group (hasic nutrient so lution), free fatty acid group (FFA,basic medium,join FFA,final concentration for 100μmol/L) and genipin group (basic medium,join genipin,final concentration for 10μmol/L). UCP2 and NF-nB phosphorylation were detected by Western blot. Corn pared with the blank control group,FFA aetivated UCP2 and NF-nB phosphorylation (P〈0.05),and Genipin inhibited UCP2 and NF-κB phosphorylation(P~0.05) in macrophages. FFA could induce the occurrence of macrophagc mitochondrial uncoup ling,and elevated NF-κB phosphorylation level.