基于ERK和NF-κB途径探讨洋金花醉茄内酯Daturataturin A抑制HaCaT细胞增殖和迁移的作用

Inhibition Effect of Daturataturin A of Datura metel L.on Proliferation and Migration of HaCaT Cells through ERK and NF-κB Pathways

目的:基于ERK和NF-κB途径,对洋金花醉茄内酯Daturataturin A(DTA)诱导HaCaT增殖、迁移、炎症及相关分子机制进行研究,从而探讨其治疗银屑病的作用机制。方法:建立人角质形成细胞(HaCaT)为表皮细胞增殖状态的模型。通过蛋白质印迹法(Western blot)、迁移实验、CCK-8细胞增殖实验等方法研究DTA治疗银屑病的药效学及其作用机制。结果:DTA抑制HaCaT增殖和迁移呈剂量和时间依赖关系;DTA可抑制IL-17诱导的HaCaT过度增殖,同时可抑制持续活化的NF-κB和下游的炎症因子。结论:DTA具有抗增殖,降低HaCaT迁移能力和抗炎效应,可以通过ERK和NF-κB途径抑制HaCaT细胞增殖和迁移,从而治疗银屑病。其机制可能是通过ERK和NF-κB途径发挥作用。

Objective:To investigate the proliferation,migration,inflammation and related molecular mechanisms of HaCaT intervened by Daturataturin A(DTA)of Datura metel L.,thus to explore its action mechanism in the treatment of psoriasis.Methods:HaCaT cell was cultured to copy the models of epidermal cell proliferation.Western blot,migration assay and CCK-8 cell proliferation assay were used to investigate the pharmacodynamics and mechanism of DTA in the treatment of psoriasis.Results:DTA inhibited the proliferation and migration of HaCaT in a dose-time dependent manner.DTA could inhibit excessive proliferation of HaCaT induced by IL-17,as well as continuously activated NF-κB and regulated inflammatory factors.Conclusion:DTA has the effect of anti-proliferation and anti-inflammation,and it can reduce HaCaT migration.The mechanism maybe related to ERK and NF-κB pathways.