背景 Nitic 氧化物(没有) 在紫外照耀导致的各种各样的煽动性的疾病,包括的晒斑和色素沉着的致病被含有。Epigallocatechin-3-gallate (EGCG ) 是在绿茶的主要有效部件并且能保护皮肤免受紫外导致损坏的伤害。这研究的目的是在可诱导的氮的氧化物 synthase (i NOS ) 上调查 EGCG 的保护的机制由在 HaCaT 房间的紫外 B (UVB ) 照耀的表示和没有产生。方法 HaCaT 房间与 UVB 30mJ/cm ~ 被照耀 2 并且有在改变集中的 EGCG 的 pretreated。i NOS mRNA 被 reversetranscriptase 聚合酶链反应(RT-PCR ) 检测,没有生产是确定的 byspectrophotometric 方法。NF-κ B P65 的表示被染色的 immunofluorescencecytochemistry 测量。结果 i NOS mRNA 的表示和产生不在 HaCaT 房间我们由 UVB 的 reincreased 照耀。EGCG 在下面以一种剂量依赖者方式调整了导致 UVB 的 i NOS mRNA 合成和 NOgeneration。NF- 的导致 UVB 的激活和κ B 低也是的 translocation 在 HaCaT 房间由 EGCG 处理调整了(P 【 0.01 ) 。结论格林茶 derived-EGCGcan 禁止并且击倒调整 NF-κ B,表示 ofiNOS mRNA 和产生的导致 UVB 的激活和 translocation 没有分别地,显示 EGCG 可以起一个保护的作用导致 fromUVB 的皮肤损坏。
Background Nitic oxide (NO) has been implicated in the pathogenesis of various inflammatory diseases, including sunburn and pigmentation induced by ultraviolet irradiation. Epigallocatechin-3-gallate (EGCG) is the major effective component in green tea and can protect skin from ultraviolet-induced damage. The purpose of this study was to investigate the protective mechanisms of EGCG on inducible nitric oxide synthase (iNOS) expression and NO generation by ultraviolet B (UVB) irradiation in HaCaT cells. Methods HaCaT cells were irradiated with UVB 30 mJ/cm^2 and pretreated with EGCG at varying concentrations. The iNOS mRNA was detected by reverse transcriptase polymerase chain reaction (RT-PCR) and NO production was quantified by spectrophotometric method. The expression of NF-κB P65 was measured by immunofluorescence cytochemistry staining. Results The expression of iNOS mRNA and generation of NO in HaCaT cells were increased by UVB irradiation. EGCG down regulated the UVB-induced iNOS mRNA synthesis and NO generation in a dose dependent manner. The UVB-induced activation and translocation of NF-κB were also down regulated by EGCG treatment in HaCaT cells (P〈0.01). Conclusions Green tea derived-EGCG can inhibit and down regulate the UVB-induced activation and translocation of NF-κB, expression of iNOS mRNA and generation of NO respectively, indicating EGCG may play a protective role from UVB-induced skin damage.