化学性低氧模拟剂氯化钴诱导人角质形成细胞炎症反应的研究

目的探讨化学性低氧模拟剂氯化钴对人皮肤角质形成细胞(HaCat)炎症反应的影响。方法用不同浓度的CoCl2处理HaCat细胞,建立化学性低氧诱导皮肤细胞损伤的实验模型后,检测细胞存活率、细胞内活性氧(ROS)、线粒体膜电位(MMP)、细胞培养液中白介素6(IL-6)和白介素8(IL-8)水平以及血红素加氧酶(HO-1)表达。结果在500～3000μmol.L-1浓度范围内,CoCl2可降低HaCat细胞存活率,且CoCl2剂量越大、细胞存活率降低越明显;2000μmol.L-1CoCl2能诱导HaCat细胞产生氧化应激反应,使胞内ROS生成增多,MMP降低;CoCl2能诱导HaCat细胞产生炎症反应,使IL-6和IL-8释放增多;1000～3000μmol.L-1CoCl2能上调HO-1的表达。结论CoCl2在诱导HaCat细胞产生氧化应激反应的同时,也能引起炎症反应,促进IL-6和IL-8的释放及HO-1表达上调。

Study on chemical hypoxia-mimetic (CoCl2) agent-induced inflammatory reaction in human keratinocytes

Aim To explore the effect of chemical hypoxia-mimetic agent,cobalt chloride(CoCl2)on inflammatory reaction in human keratinocytes(HaCat cells).Methods After HaCat cells were treated with CoCl2 at different concentrations to set up a chemical hypoxia-induced cell model of skin injury,cell viability,intracellular reactive oxygen species(ROS),mitochondrial membrane potential(MMP),the levels of both interleukin 6(IL-6)and interleukin 8(IL-8)as well as the expression of heme oxygenase-1(HO-1)were detected.Results The viability of HaCat cells was reduced by CoCl2 at the concentrations from 500 to 3 000 μmol·L-1,and the higher CoCl2 doses,the lower cell viability was.CoCl2 induced oxidative stress reaction(increasing ROS production and decreasing MMP).CoCl2 induced inflammatory reaction,enhancing the release of IL-6 and IL-8.CoCl2 at concentrations from 1 000 to 3 000 μmol·L-1 upregulated HO-1 expression in HaCat cells.Conclusion CoCl2 induces not only oxidative stress,but also inflammatory reaction,increasing the release of both IL-6 and IL-8,as well as HO-1 expression.