摘要
目的:探讨茶多酚的活性单体表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)对紫外线辐射氧化损伤的保护机制。方法:用722分光光度计测定培养的人皮肤成纤维细胞上清液中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性,以及脂质过氧化产物丙二醛(MDA)的含量;采用逆转录-聚合酶链反应(RT-PCR)方法测定成纤维细胞合成基质金属蛋白酶1(MMP1)以及其组织抑制因子-1(TIMP-1)的mRNA表达水平。结果:EGCG可以减少中波紫外线(UVB)辐射引起的丙二醛沉积,增加抗氧化酶的活性;并且可以抑制UVB诱导的MMP1mRNA表达,减少胶原蛋白的降解。对TIMP-1的表达则没有观察到显著变化。结论:EGCG可以对UVB辐射损伤的体外培养成纤维细胞起到保护作用。
Objective:To explore the protection mechanism of epigallocatechin-3-gallate(EGCG),a major green tea catechin,from ultraviolet B induced fibroblast damage.Methods:The activity of antioxidases and the content of malondialdehyde(MDA)in the culture medium were measured by biochemical assay;the mRNA of matrix metalloproteinase1(MMP-1)and tis-sue inhibitor of metalloproteinase(TIMP-1)were determined by reverse transcription polymerase chain reaction(RT-PCR).Re -sults:EGCG reduced the MDA accumulation induced by ultraviolet B(UVB)and increased the activity of antioxidases.The mRNA expression of MMP-1induced by UVB irradiation was down-regulated by EGCG.However,no great change was ob-served in the expression of TIMP-1before and after the UVB irradiation.Conclusion:EGCG has potential protective effects from UVB induced damage on cultured fibroblasts.
出处
《临床皮肤科杂志》
CAS
CSCD
北大核心
2003年第6期315-317,共3页
Journal of Clinical Dermatology
基金
国家自然科学基金(项目编号:3027119)
