首页> 外文期刊>Journal of the Korean Society for Applied Biological Chemistry >The Protective Effect of Glycitin on UV-induced Skin Photoaging in Human Primary Dermal Fibroblast
【24h】

The Protective Effect of Glycitin on UV-induced Skin Photoaging in Human Primary Dermal Fibroblast

机译:甘草糖素对紫外线诱导的人原代皮肤成纤维细胞皮肤光老化的保护作用

获取原文
获取原文并翻译 | 示例
           

摘要

Exposure of strong and repeated UV on the skin leads to skin aging, characterized with wrinkling, sagging, dyspigmentation, and laxity. Numerous studies revealed that Matrix metalloproteinases are related to skin aging and functions as degrading enzyme of various types of collagen. Here, we attempted to evaluate the effectiveness of glycitin (4'-hydroxy-6-methoxy-isoflavone-7-D-glucoside) on skin aging and mechanisms of action in UV-irradiated human dermal fibroblasts. Especially we focused on the expression of Matrix metalloproteinase-1 (MMP-1), which degrades procollagen type-I in dermis, by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Western blot, and reverse transcription polymerase chain reaction in cell lysates or media. Our results showed that glycitin increased the viability of human dermal fibroblast and alleviated MMP-1 expression caused by UV irradiation. In addition, synthesis of type-I collagen was increased and UV-induced phosphorylation of ERK/JNK/p38 was decreased in dose-dependent manners. Taken together, we demonstrated that treatment with glycitein have a protective effect on skin aging by inhibiting of MMP-1 and increasing of collagen through ERK/JNK/P38 down-regulation, which may be mediated by the inhibition of ERK, JNK, and p38 mitogen-activated protein kinases. We suggest that glycitin is a potential agent for the treatment of skin ageing
机译:暴露在皮肤上的强力且反复的紫外线会导致皮肤老化,其特征是起皱,松弛,色素沉着和松弛。大量研究表明,基质金属蛋白酶与皮肤衰老有关,并起各种胶原蛋白的降解酶的作用。在这里,我们试图评估glycitin(4'-羟基-6-甲氧基-异黄酮-7-D-葡萄糖苷)对皮肤衰老的有效性以及在紫外线照射的人类皮肤成纤维细胞中的作用机理。特别是,我们通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴化物测定法研究了基质金属蛋白酶-1(MMP-1)的表达,该酶降解真皮中的I型胶原蛋白。印迹和逆转录聚合酶链反应在细胞裂解液或培养基中。我们的研究结果表明,glycitin可提高人皮肤成纤维细胞的活力,并减轻由紫外线照射引起的MMP-1表达。另外,I型胶原蛋白的合成以剂量依赖性方式增加,并且UV诱导的ERK / JNK / p38磷酸化降低。综上所述,我们证明了用糖蛋白治疗可以通过抑制MMP-1和通过ERK / JNK / P38下调来增加胶原蛋白对皮肤衰老的保护作用,这可能是由于抑制ERK,JNK和p38介导的。丝裂原激活的蛋白激酶。我们建议,glycitin是治疗皮肤衰老的潜在药物

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号