Treatment of green tea polyphenols in hydrophilic cream prevents UVB-induced oxidation of lipids and proteins, depletion of antioxidant enzymes and phosphorylation of MAPK proteins in SKH-1 hairless mouse skin.
Treatment of green tea polyphenols in hydrophilic cream prevents UVB-induced oxidation of lipids and proteins, depletion of antioxidant enzymes and phosphorylation of MAPK proteins in SKH-1 hairless mouse skin.
复制标题
亲水霜中的绿茶多酚处理可防止 SKH-1 无毛小鼠皮肤中 UVB 诱导的脂质和蛋白质氧化、抗氧化酶消耗以及 MAPK 蛋白质磷酸化。
DOI：
10.1093/carcin/bgg025
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发表时间：
2003
期刊：
影响因子：
4.7
通讯作者：
Katiyar,SantoshK
中科院分区：
文献类型：
--
作者：
Vayalil,PraveenK;Elmets,CraigA;Katiyar,SantoshK
近年来，植物补充剂的使用受到了极大的关注，以保护人类皮肤免受太阳紫外线（UV）辐射的不良生物效应。来自绿色茶的多酚是其中之一，并且已经在动物模型中显示出防止光致癌作用，但是其光保护机制还不太清楚。为了确定小鼠模型中光保护的机制，局部处理来自绿色茶的多酚（GTP）或其最具化学预防性的成分（-）-表没食子儿茶素-3-没食子酸酯（EGCG）。（1 mg/cm 2皮肤面积），在单次给药前溶于亲水性软膏USP中（180 mJ/cm 2）或多次UVB暴露（180 mJ/cm 2，每天10天）导致显着防止UVB诱导的抗氧化酶，如谷胱甘肽过氧化物酶的消耗（78- 100%，P < 0.005-0.001）、过氧化氢酶（51- 92%，P < 0.001）、谷胱甘肽（87- 100%，P < 0.005）。以脂质过氧化（76- 95%，P < 0.001）和蛋白质氧化（67- 75%，P> 0.001）为指标，EGCG或GTP处理也能抑制UVB诱导的氧化应激。此外，为了描述UVB诱导的氧化应激与细胞信号传导途径的抑制，EGCG处理小鼠皮肤导致UVB辐射诱导的MAPK家族的ERK 1/2（16-95%）、JNK（46-100%）和p38（100%）蛋白的磷酸化以时间依赖性方式显著抑制。在多次UVB照射小鼠皮肤中，观察到相同的EGCG或GTP对MAPK家族蛋白磷酸化的光保护作用。在饮用水（d.w.）中给予的GTP的光保护功效(0.2%，w/v），并与局部处理的EGCG和GTP进行比较。d.w.中GTP的治疗抗氧化酶活性降低（44- 61%，P < 0.01-0.001），氧化应激水平降低（33- 71%，P < 0.01），MAPK家族的ERK 1/2、JNK和p38蛋白磷酸化水平降低，但其光保护作用不及EGCG和GTP。GTP在d.w.中的较小光保护功效。可能是由于其在皮肤靶细胞中生物利用度较低。总之，在本研究中首次测试了绿色茶多酚的霜基制剂以探索其用于人类的可能性，并且从该体内研究获得的数据进一步表明GTP可用于减弱太阳UVB光诱导的氧化应激介导的和MAPK引起的人类皮肤疾病。
The use of botanical supplements has received immense interest in recent years to protect human skin from adverse biological effects of solar ultraviolet (UV) radiation. The polyphenols from green tea are one of them and have been shown to prevent photocarcinogenesis in animal models but their mechanism of photoprotection is not well understood. To determine the mechanism of photoprotection inin vivomouse model, topical treatment of polyphenols from green tea (GTP) or its most chemopreventive constituent (−)-epigallocatechin-3-gallate (EGCG) (1 mg/cm2skin area) in hydrophilic ointment USP before single (180 mJ/cm2) or multiple UVB exposures (180 mJ/cm2, daily for 10 days) resulted in significant prevention of UVB-induced depletion of antioxidant enzymes such as glutathione peroxidase (78–100%,P< 0.005–0.001), catalase (51–92%,P< 0.001) and glutathione level (87–100%,P< 0.005). Treatment of EGCG or GTP also inhibited UVB-induced oxidative stress when measured in terms of lipid peroxidation (76–95%,P< 0.001), and protein oxidation (67–75%,P> 0.001). Further, to delineate the inhibition of UVB-induced oxidative stress with cell signaling pathways, treatment of EGCG to mouse skin resulted in marked inhibition of a single UVB irradiation-induced phosphorylation of ERK1/2 (16–95%), JNK (46–100%) and p38 (100%) proteins of MAPK family in a time-dependent manner. Identical photoprotective effects of EGCG or GTP were also observed against multiple UVB irradiation-induced phosphorylation of the proteins of MAPK familyin vivomouse skin. Photoprotective efficacy of GTP given in drinking water (d.w.) (0.2%, w/v) was also determined and compared with that of topical treatment of EGCG and GTP. Treatment of GTP in d.w. also significantly prevented single or multiple UVB irradiation-induced depletion of antioxidant enzymes (44–61%,P< 0.01–0.001), oxidative stress (33–71%,P< 0.01) and phosphorylation of ERK1/2, JNK and p38 proteins of MAPK family but the photoprotective efficacy was comparatively less than that of topical treatments of EGCG and GTP. Lesser photoprotective efficacy of GTP in d.w. in comparison with topical application may be due to its less bioavailability in skin target cells. Together, for the first time a cream based formulation of green tea polyphenols was tested in this study to explore the possibility of its use for the humans, and the data obtained from thisin vivostudy further suggest that GTP could be useful in attenuation of solar UVB light-induced oxidative stress-mediated and MAPK-caused skin disorders in humans.