芍药苷抑制NF-κB通路减少银屑病HaCaT细胞炎症的作用研究

Paeoniflorin Inhibiting NF-κB Pathway and Reducing Inflammation of HaCaT Cells in Treatment of Psoriasis

目的:观察芍药苷(TGP)对脂多糖(LPS)诱导的银屑病样角质形成(HaCaT)细胞模型的作用,并分析其作用机制。方法:使用LPS浓度为1μg/mL的DMEM高糖培养基刺激HaCaT细胞24 h为模型组(LPS),TGP干预为芍药苷组(TGP),同时设立空白组(CON)。应用CCK-8法评估TGP的毒性,蛋白质印迹法观察p-IKB/IKB、p-NF-κB/NF-κB比值,免疫荧光法测定IL-1β表达量的变化,并进行JC-1线粒体膜电位水平及ROS活性氧检测。结果:与模型组比较,芍药苷可降低HaCaT细胞中IL-1β表达量;降低p-IKB/IKB、p-NF-κB/NF-κB的比值;减少细胞内活性氧(ROS)过度累积;维持线粒体膜电位的正常水平。结论:芍药苷通过抑制NF-κB通路来减少炎症因子的释放,从而减缓银屑病进展。芍药苷对HaCaT细胞的抑制作用可能是其治疗银屑病的机制之一。

Objective:To observe the effect of paeoniflorin on psoriatic-like keratinocytes(HaCaT)induced by lipopolysaccharide(LPS)and to explore its mechanism.Methods:HaCaT cells were cultured in DMEM high glucose medium with LPS concentration of 1μg/mL for 24 h.The toxicity of paeoniflorin was evaluated by CCK-8.The ratios of p-IKB/IKB and p-NF-κB/NF-κB were calculated after Western blotting observation.The expression of IL-1βwas detected by immunofluorescence.The level of JC-1 mitochondrial membrane potential was observed and the ROS activity was detected.Results:Compared with those in the model group,paeoniflorin decreased the expression of IL-1β,reduced the ratios of p-IKB/IKB and p-NF-κB/NF-κB,alleviated the accumulation of reactive oxygen species(ROS)in HaCaT cells,and maintained the normal level of mitochondrial membrane potential.Conclusion:Paeoniflorin may reduce the release of inflammatory factors by inhibiting NF-κB pathway,thus to slow down the progression of psoriasis.These results suggest that the inhibitory effect of paeoniflorin on HaCaT cells may be one of the mechanisms of paeoniflorin in treating psoriasis.