Department of Dermatology, University of Alabama at Birmingham, 35294, USA.
Cancer Prev Res (Phila). 2010 Feb;3(2):179-89. doi: 10.1158/1940-6207.CAPR-09-0044. Epub 2010 Jan 26.
UV radiation-induced immunosuppression has been implicated in the development of skin cancers. Green tea polyphenols (GTP) in drinking water prevent photocarcinogenesis in the skin of mice. We studied whether GTPs in drinking water (0.1-0.5%, w/v) prevent UV-induced immunosuppression and (if so) potential mechanisms of this effect in mice. GTPs (0.2% and 0.5%, w/v) reduced UV-induced suppression of contact hypersensitivity (CHS) in response to a contact sensitizer in local (58-62% reductions; P < 0.001) and systemic (51-55% reductions; P < 0.005) models of CHS. Compared with untreated mice, GTP-treated mice (0.2%, w/v) had a reduced number of cyclobutane pyrimidine dimer-positive (CPD(+)) cells (59%; P < 0.001) in the skin, showing faster repair of UV-induced DNA damage, and had a reduced (2-fold) migration of CPD(+) cells from the skin to draining lymph nodes, which was associated with elevated levels of nucleotide excision repair (NER) genes. GTPs did not prevent UV-induced immunosuppression in NER-deficient mice but significantly prevented it in NER-proficient mice (P < 0.001); immunohistochemical analysis of CPD(+) cells indicated that GTPs reduced the numbers of UV-induced CPD(+) cells in NER-proficient mice (P < 0.001) but not in NER-deficient mice. Southwestern dot-blot analysis revealed that GTPs repaired UV-induced CPDs in xeroderma pigmentosum complementation group A (XPA)-proficient cells of a healthy person but did not in XPA-deficient cells obtained from XPA patients, indicating that a NER mechanism is involved in DNA repair. This study is the first to show a novel NER mechanism by which drinking GTPs prevents UV-induced immunosuppression and that inhibiting UV-induced immunosuppression may underlie the chemopreventive activity of GTPs against photocarcinogenesis.
紫外线辐射诱导的免疫抑制与皮肤癌的发展有关。饮水中的绿茶多酚(GTP)可预防小鼠皮肤的光致癌作用。我们研究了饮水中的 GTP(0.1-0.5%,w/v)是否可预防 UV 诱导的免疫抑制,以及(如果可以)其在小鼠中的潜在作用机制。GTP(0.2%和 0.5%,w/v)降低了局部(58-62%的降低;P < 0.001)和全身(51-55%的降低;P < 0.005)模型中对接触致敏原的接触超敏反应(CHS)的 UV 诱导抑制。与未经处理的小鼠相比,GTP 处理的小鼠(0.2%,w/v)皮肤中嘧啶二聚体阳性(CPD(+))细胞的数量减少(59%;P < 0.001),表明 UV 诱导的 DNA 损伤修复更快,并且 CPD(+)细胞从皮肤向引流淋巴结的迁移减少(2 倍),这与核苷酸切除修复(NER)基因水平升高有关。GTP 不能预防 NER 缺陷型小鼠的 UV 诱导的免疫抑制,但在 NER 功能正常的小鼠中显著预防(P < 0.001);CPD(+)细胞的免疫组织化学分析表明,GTP 减少了 NER 功能正常的小鼠中 UV 诱导的 CPD(+)细胞的数量(P < 0.001),但在 NER 缺陷型小鼠中则没有。西南印迹分析显示,GTP 修复了来自健康个体的 XPA 功能正常细胞中的 UV 诱导的 CPD,但不能修复来自 XPA 患者的 XPA 缺陷细胞中的 CPD,表明 NER 机制参与了 DNA 修复。这项研究首次表明,通过饮用 GTP 预防 UV 诱导的免疫抑制的新的 NER 机制,并且抑制 UV 诱导的免疫抑制可能是 GTP 预防光致癌作用的化学预防活性的基础。