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作 者:魏政 苏慧琳 匡海学[1] WEI Zheng;SU Huilin;KUANG Haixue(Heilongjiang University of Chinese Medicine, Harbin 150040, China;Guangdong Pharmaceutical University, Guangzhou 510006, China)
机构地区:[1]黑龙江中医药大学,黑龙江哈尔滨150040 [2]广东药科大学中药学院,广东广州510006
出 处:《中医药信息》2020年第4期1-8,共8页Information on Traditional Chinese Medicine
基 金:国家重点基础研究发展计划(973计划)(2013CB531801)。
摘 要: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.
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