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为检测AICAR激活及Compound C抑制脂肪细胞AMPK磷酸化后对NF-κΒ的磷酸化活性的影响,探讨肥胖启动炎症的分子机制。将3T3-L1细胞诱导为成熟脂肪细胞后,实验分3个处理:基础培养液组(对照组)、实验组(基础培养液组分别加入AICAR和Compound C)。运用Western blot检测药物干预后AMPK与NF-κΒ的磷酸化水平。结果显示,AICAR培养1h脂肪细胞内AMPK磷酸化水平增加,Compound C培养1h脂肪细胞内AMPK磷酸化水平降低,差异有统计学意义(P<0.05)。AICAR培养1h脂肪细胞内NF-κΒ磷酸化水平降低,Compound C培养1h脂肪细胞NF-κΒ磷酸化水平增高,差异有统计学意义(P<0.05)。由此可知,AMPK活性与NF-κΒ活性呈一定的负相关,AMPK可抑制NF-κΒ信号,肥胖导致炎症可能是AMPK活性降低引发NF-κΒ信号活性增强有关。
To investigate the effect of AICAR activation and Compound C on the phosphorylation of NF-κB induced by AMPK phosphorylation in adipocytes, the molecular mechanism of obesity-induced inflammation was explored. After 3T3-L1 cells were induced to mature adipocytes, the experiment was divided into 3 treatments: basal medium group (control group) and experimental group (basal medium group added AICAR and Compound C respectively). Western blot was used to detect the phosphorylation of AMPK and NF-κB after drug intervention. The results showed that the phosphorylation of AMPK was increased in adipocytes cultured with AICAR for 1 h, and the phosphorylation of AMPK was decreased in adipocytes cultured with Compound C for 1 h (P <0.05). The level of NF-κB phosphorylation in adipocytes cultured with AICAR for 1h was lower, and the phosphorylation level of NF-κB in adipocytes increased 1h after treatment with Compound C (P <0.05). This shows that AMPK activity and NF-κΒ activity was negatively correlated, AMPK can inhibit NF-κΒ signal, obesity-induced inflammation may be related to decreased activity of AMPK trigger NF-κΒ signal activity.