Cancer chemopreventive effects of polyphenols from green tea (GTP) in mouse models of photocarcinogenesis are established. The present study is extended from mouse model to human system in vivo to determine the effect of topical application of GTP to human individuals against UV light-induced DNA damage in the form of cyclobutane pyrimidine dimers (CPDs) in the skin. UVB-induced CPDs were detected by immunohistochemical technique using monoclonal antibodies to thymine dimers. With the gradual increase in UVB dose, both erythema response and CPD formation in the skin was increased. GTP treatment inhibited both UVB-induced erythema response as well as CPD formation. Topical treatment with GTP (approximately 1 mg/cm2 of skin area) 20 min before human buttock skin (sun-protected site) exposure to UVB inhibited CPD formation in epidermis by 81, 70, 60, and 60% at 0.5, 1.0, 2.0, and 4.0 minimal erythema dose of UV exposure, respectively. Treatment of human skin with varying doses of GTP (1-4 mg/2.5 cm2 of skin area) before a single dose of UVB exposure (4.0 minimal erythema dose) decreased dose dependently the formation of UVB-induced CPDs in both epidermis and dermis. The inhibition of UVB-induced CPDs by GTP treatment may be, at least in part, responsible for the inhibition of photocarcinogenesis. Our data suggest that GTP may be used as a novel chemopreventive candidate and possible strategy to reduce UV-induced skin cancer risk in the human population.

译文

:建立了绿茶(GTP)中的多酚在光致癌小鼠模型中的化学预防作用。本研究从小鼠模型扩展到体内的人体系统,以确定局部应用GT​​P对人体产生的抗UV光诱导的DNA伤害,其形式为皮肤中的环丁烷嘧啶二聚体(CPDs)。使用针对胸腺嘧啶二聚体的单克隆抗体,通过免疫组织化学技术检测了UVB诱导的CPD。随着UVB剂量的逐渐增加,皮肤中的红斑反应和CPD形成均增加。 GTP处理既抑制了UVB引起的红斑反应,又抑制了CPD的形成。在人臀部皮肤(防晒部位)暴露于UVB之前20分钟,用GTP(约1 mg / cm2皮肤面积)局部治疗在0.5、1.0、2.0、81、70、60和60%抑制表皮中的CPD形成。和分别为4.0的紫外线最小红斑剂量。在单剂量的UVB暴露(最小红斑剂量为4.0)之前,使用不同剂量的GTP(1-4 mg / 2.5 cm2皮肤面积)治疗人的皮肤,剂量会减少,这取决于表皮和真皮中UVB诱导的CPD的形成。通过GTP处理抑制UVB诱导的CPD可能至少部分负责光致癌作用的抑制。我们的数据表明,GTP可用作新型化学预防候选药物,并可能是降低人群中紫外线诱发的皮肤癌风险的策略。

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