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作 者:谢青[1] 颜会兰[1] 李应全[2] 王进[2] 王菊英[2]
机构地区:[1]山东大学齐鲁医院药学部,山东济南250012 [2]山东大学医学院药理学研究所,山东济南250012
出 处:《药学学报》2007年第10期1050-1053,共4页Acta Pharmaceutica Sinica
基 金:山东省卫生厅科技发展计划项目(2005HW084).
摘 要:观察依托泊苷(etoposide,VP-16)对小鼠变应性接触性皮炎(allergic contact dermatitis,ACD)的抗炎作用并探讨其可能的机制。采用2,4-二硝基氟苯(dinitrofluorobenzene,DNFB)致小鼠ACD模型,观察VP-16给药后皮肤炎症反应程度,应用放射免疫分析法测定血清中肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)和白细胞介素-10(interleukin-10,IL-10)的水平,免疫组化法测定皮肤中细胞间粘附分子(intercellular adhesion molecule,ICAM-1)的表达。结果显示,VP-16可显著降低炎性细胞浸润,减轻炎症反应程度,明显降低血清中炎症促发因子TNF-α的水平及皮肤中ICAM-1的表达。VP-16可以有效抑制DNFB诱发的小鼠ACD,可能通过对某些细胞因子的抑制而发挥作用。This study is to observe the inhibition of etoposide on allergic contact dermatitis (ACD) and explore its possible mechanism of action. Dinitrofluorobenzene was used to induce the allergic contact dermatitis in mouse ear. Three groups of animals were orally administrated with different doses of VP-16 (5, 10, and 20 mg . kg^-1 ) , separately, for six days. The degree of skin inflammatory reaction was observed by optical microscope. Expression of intercellular adhesion molecule (ICAM-1) was detected by immunohistochemical staining. Radioimmunoassay was applied to measure the serum level of tumor necrosis factor-or (TNF-α) and interleukin-10 (IL-10). VP-16 significantly decreased inflammatory cell infiltration and the degree of infiltration reaction, and decreased the level of TNF-α in serum and the expression of ICAM-I in skin. VP-16 can significantly inhibit allergic contact dermatitis induced by DNFB. This therapeutic effect of VP-16 on murine ACD may be due to inhibiting expression of some cytokines.
分 类 号:R963[医药卫生—微生物与生化药学]
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