目的：：明确 NB－UVB 对 HaCaT 细胞 CCL22的影响。方法：常规培养后的 HaCaT 细胞分为两组,一组给予不同剂量 NB－UVB (0、100、200、400 mJ/ cm2)照射；一组给予 NF－κB 抑制剂 PDTC (1、12.5、25μmol/ L)预处理后再进行 NB－UVB 照射,采用 Real－time PCR 及 ELISA 检测 CCL22表达；采用 Western blot 方法检测 NF－κB p65磷酸化水平。结果： CCL22表达和 NF－κB p65磷酸化的水平随着 NB－UVB 照射剂量增强而上调；PDTC 处理后,NB－UVB 诱导的角质形成细胞 CCL22表达及和 NF－κB p65磷酸化水平较直接给予 NB－UVB 明显下调,且 PDTC 浓度越高越明显。结论： NB－UVB 照射可能通过激活 NF－κB 信号通路促进角质形成细胞 CCL22表达及分泌。%Objective: To determine the effects of NB-UVB on the expression of CCL22 from HaCaT cells. Methods: The cultrued HaCaT cells were divided into two groups. The HaCaT cells in one group were treated with different dose of NB-UVB (0,100,200,400 mJ/ cm2 ) and those in the second group were treated with NB-UVB (400 mJ/ cm2 ) after the pretreatment with PDTC. The expression of CCL22 was detected by Real-time PCR and ELISA. The level of NF-κB p65 phosphorylation was detected by western blot. Results: The expression of CCL22 and the level of NF-κB p65 phosphorylation in HaCaT cells treated with NB-UVB were increased as the dose of of NB-UVB was increasing. The expression of CCL22 and the level of NF-κB p65 phosphorylation in HaCaT cells pretreated by PDTC were lower than those treated with NB-UVB only and the higher the concentration of PDTC, the effects were more obvious. Conclusion: The CCL22 expression induced by NB-UVB in keratinocytes may through activation of NF-κB pathway.
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