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作 者:肖汀[1] 吴江[1] 吴剑[1] 王雅坤[1] 何春涤[1] 陈洪铎[1]
机构地区:[1]中国医科大学附属第一医院皮肤科,沈阳110001
出 处:《中华皮肤科杂志》2008年第2期115-117,共3页Chinese Journal of Dermatology
基 金:国家自然科学基金(30400389)
摘 要:目的观察UVA、窄谱UVB(NB-UVB)和三种免疫抑制剂对HaCaT细胞分泌IFN-γ诱生的单核因子(CXCL9/Mig)的影响。方法用ELISA检测不同剂量UVA、NB-UVB以及不同浓度的地塞米松、甲氨蝶呤和雷公藤内酯醇作用后培养24h的HaCaT细胞上清中CXCL9/Mig水平。结果UVA(2,4,6,8J/cm^2)、NB-UVB(0.1J/cm^2)、地塞米松(0.001,0.01,0.1,10ng/mL)、甲氨蝶呤(1,10ng/mL)和雷公藤内酯醇(0.01,0.1,1ng/mL)均显著抑制HaCaT细胞分泌CXCL9/Mig(P〈0.05)。结论UVA、NB-UVB、地塞米松、甲氨蝶呤和雷公藤内酯醇对Th1占主导的炎症性皮肤病的治疗机制可能均与其抑制角质形成细胞分泌CXCL9/Mig有关。Objective To investigate the effects of ultraviolet A (UVA), narrow-band ultraviolet B (NB-UVB) and three immunosupprcssants on CXCL9/Mig secretion by a human kcratinocytc cell line, HaCaT. Methods Enzyme-linked immunosorbcnt assay (ELISA) was carried out to detect the levels of CXCL9/Mig in the culture supcrnatant of HaCaT cells, which had bccn cultured for 24 hours after being exposed to various doses or concentrations of UVA, NB-UVB, dcxamcthasonc, mcthotrcxatc and triptolidc. Results The CXCL9/Mig secretion by HaCaT cells was significantly inhibited by UVA (2, 4, 6, 8 J/cm^2), NB-UVB (0.1 J/cm^2), dcxamcthasonc (0.001, 0.01, 0.1, 1, 10 ng/mL), triptolidc (0.01, 0.1, 1 ng/mL) and mcthotrcxatc (1, 10 ng/mL), respectively (P 〈 0.05 or 0.01 ). Conclusion The therapeutic mechanisms of UVA, NB-UVB, dcxamcthasonc, mcthotrcxatc and triptolidc for Thl-dominated skin diseases may bc associated with their inhibitory effects on CXCL9/Mig secretion by kcratinocytcs.
关 键 词:地塞米松 甲氨蝶呤 CXCL9/Mig HacaT细胞 雷公藤内酯 紫外线
分 类 号:R758.65[医药卫生—皮肤病学与性病学]
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