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首页> 美国卫生研究院文献>other >Inhibition of UVB-Induced Skin Tumor Development by Drinking Green Tea Polyphenols is Mediated Through DNA Repair and Subsequent Inhibition of Inflammation
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Inhibition of UVB-Induced Skin Tumor Development by Drinking Green Tea Polyphenols is Mediated Through DNA Repair and Subsequent Inhibition of Inflammation

机译：喝绿茶多酚对UVB诱导的皮肤肿瘤发育的抑制作用是通过DNA修复和随后的炎症抑制作用介导的。

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Consumption of green tea polyphenols (GTPs) in drinking water prevents photocarcinogenesis in mice; however, the molecular mechanisms underlying this effect have not been fully elucidated. Using interleukin (IL)-12p40 knockout (IL-12-KO) mice and their wild-type counterparts and an established photocarcinogenesis protocol, we found that although administration of GTPs (0.2%, w/v) in drinking water significantly reduced UVB-induced tumor development in wild-type mice, this treatment had a non-significant effect in IL-12-KO mice. GTPs resulted in reduction in the levels of markers of inflammation (COX-2, PGE2, PCNA, cyclin D1) and proinflammatory cytokines (TNF-α, IL-6, IL-1β) in chronically UVB-exposed skin and skin tumors of wild-type mice but less effective in IL-12p40-KO mice. UVB-induced DNA damage (cyclobutane pyrimidine dimers) was resolved rapidly in GTPs-treated wild-type mice than untreated wild-type mice and this resolution followed the same time course as the GTPs-induced reduction in the levels of inflammatory responses. This effect of GTPs was less pronounced in IL-12-KO mice. The above results were confirmed by treatment of IL-12-KO mice with murine rIL-12 and treatment of wild-type mice with neutralizing anti-IL-12 antibody. To our knowledge this is previously unreported that prevention of photocarcinogenesis by GTPs is mediated through IL-12-dependent DNA repair and a subsequent reduction in skin inflammation.
机译：饮用水中的绿茶多酚（GTP）摄入会阻止小鼠的光致癌作用。但是，尚未完全阐明这种作用的分子机制。使用白介素（IL）-12p40敲除（IL-12-KO）小鼠及其野生型对应小鼠和已建立的光致癌方案，我们发现尽管在饮用水中施用GTP（0.2％，w / v）可以显着降低UVB-由于在野生型小鼠中诱导了肿瘤的发展，这种治疗对IL-12-KO小鼠没有显着影响。 GTP导致慢性UVB暴露的皮肤和野生型皮肤肿瘤中炎症标志物（COX-2，PGE2，PCNA，细胞周期蛋白D1）和促炎细胞因子（TNF-α，IL-6，IL-1β）的水平降低型小鼠，但在IL-12p40-KO小鼠中效果较差。与未经处理的野生型小鼠相比，经GTP处理的野生型小鼠中UVB诱导的DNA损伤（环丁烷嘧啶二聚体）得到了快速解决，并且这种消退与GTP诱导的炎症反应水平降低的时间相同。 GTP的这种作用在IL-12-KO小鼠中不太明显。通过用鼠rIL-12治疗IL-12-KO小鼠和用中和性抗IL-12抗体治疗野生型小鼠证实了以上结果。据我们所知，以前尚未报道过GTP预防光致癌作用是通过依赖IL-12的DNA修复和随后的皮肤炎症减轻来介导的。

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