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Protective Effect of Dibenzoylmethane on Chemically- and UV Light-Induced Skin, Inflammation, Sunburn Lesions, and Skin Carcinogenesis in Mice

机译:二苯甲酰甲烷对小鼠化学和UV光诱导皮肤,炎症,晒伤病变和小鼠皮肤致癌作用的保护作用

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Dibenzoylmethane (DBM) is a minor constituent of licorice and an analogue of curcumin. We previously reported that feeding 1% DBM in the diet strongly inhibited 7,12-dimethylbenzyla[a]anthracene (DMBA)-induced mammary tumorigenesis and formation of leukemias/lymphomas in Sencar mice). In this report, we show that topical application of DBM to the backs of mice inhibited chemical- and ultraviolet light (UV)-induced inflammation, sunburn lesions, and formation of skin tumors in mice. Topical application of DBM inhibited TPA-induced edema of mouse ears and skin tumor promotion in CD-1 mice in a dose-dependent manner. Topical application of 3 - 10 μmol DBM with 5 nmol TPA twice weekly for 16 weeks in CD-1 mice previously treated with DMBA inhibited the number of skin tumors per mouse by 65 - 93%, and percent of mice with tumors was inhibited by 29 - 50%.. Topical application of 10 μmol DBM with mirex (a non-TPA type tumor promoter) 3 times a week for 18 weeks in DMBA-initiated mice inhibited the mirex-induced number of tumors per mouse by 63%. DBM also strongly inhibited UV-induced skin sunburn lesions and formation of skin tumors in SKH-1 mice. Topical application of 10 μmol DBM to SKH-1 mice previously initiated with DMBA at 10 min prior to each UV (30 mJ/cm~2) irradiation twice a week for 34 weeks inhibited the number of skin tumors per mouse by 91%. Percent of mice with skin tumors was reduced by 44%. In complete UV skin tumorigenic model, topical application of 10 umol DBM at 10 min before each UV (30 mJ/cm~2) irradiation twice weekly for 34 weeks inhibited the number of skin tumors per mouse by 96%, and percent of mice with tumors was decreased by 48%. Our results indicated that DBM strongly inhibited both chemical- and UV-induced skin inflammation, sunburn lesions and skin tumorigenesis in mice.
机译:二苯甲酰甲烷(DBM)是甘草的次要组成和姜黄素的类似物。我们以前报道,在饮食中喂养1%DBM强烈抑制7,12-二甲基苄基[A]蒽(DMBA)诱导的乳腺瘤瘤和在Sencar小鼠中的白血病/淋巴瘤的形成)。在本报告中,我们认为DBM的局部将DBM施用于小鼠的背面抑制化学和紫外线(UV)诱导的炎症,晒伤病变和在小鼠中形成皮肤肿瘤。 DBM的局部施用抑制CD-1小鼠的TPA诱导的小鼠的水肿和皮肤肿瘤促进剂以剂量依赖性方式。在先前用DMBA处理的CD-1小鼠中每周施用3-10μmolDBM的局部施用3-10μmolDBM,6周,以先前用DMBA治疗的CD-1小鼠抑制每只小鼠的皮肤肿瘤数量65-93%,29℃抑制肿瘤的百分比 - 50%。在DMBA引发的小鼠中每周18周局部施用10μmoldBM的麦克风(非TPA型肿瘤促进剂)3次,抑制每只小鼠的MiREX诱导的肿瘤数量63%。 DBM也强烈抑制紫外线诱导的皮肤晒伤病变,在SKH-1小鼠中形成皮肤肿瘤。在每一周两次施用每周两次,每次紫外线(30mJ / cm〜2)辐射后10分钟,局部施用10μmoldBm至skh-1小鼠的SkH-1小鼠。34周抑制每只小鼠的皮肤肿瘤数量为91%。皮肤肿瘤的小鼠百分比减少了44%。在完全紫外线皮肤致瘤模型中,在每次UV(30mJ / cm〜2)前10分钟的局部施用10μm,每周两次照射34周,抑制每只小鼠的皮肤肿瘤数量为96%,以及小鼠的百分比肿瘤降低了48%。我们的结果表明,DBM强烈抑制了小鼠中的化学和紫外线诱导的皮肤炎症,晒伤病变和皮肤肿瘤瘤。

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