首页> 外文OA文献 >Potential Anti-Skin Aging Effect of (-)-Catechin Isolated from the Root Bark of Ulmus davidiana var. japonica in Tumor Necrosis Factor-α-Stimulated Normal Human Dermal Fibroblasts
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Potential Anti-Skin Aging Effect of (-)-Catechin Isolated from the Root Bark of Ulmus davidiana var. japonica in Tumor Necrosis Factor-α-Stimulated Normal Human Dermal Fibroblasts

机译:( - ) - 从Ulmus Davidiana var的根吠肠中分离出的抗皮肤老化效应。肿瘤坏死因子-α-刺激的正常人皮肤成纤维细胞的粳稻

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摘要

Reactive oxygen species (ROS) are generated during skin aging, including intrinsic (chronologic aging) and extrinsic aging (photoaging). Therefore, antioxidants that inhibit ROS generation can delay skin aging. In this study, we evaluated the potential anti-skin aging effect of (-)-phenolic compounds isolated from the root bark of Ulmus davidiana var. japonica. We preferentially investigated the possible preventive effects of isolates against the degradation of skin extracellular matrix. Among the isolates, (-)-catechin suppressed the activity of collagenase MMP-1, and reversed the degradation of collagen induced by tumor necrosis factor-α (TNF-α) in normal human dermal fibroblast. This action mechanism of (-)-catechin was validated by the suppression of tumor necrosis factor-α-induced accumulation of ROS and activation of mitogen-activated protein kinases, protein kinase B (Akt), and cyclooxygenase-2 (COX-2). The proinflammatory cytokines upregulate inflammatory reactions, and ultimately promote aging-related reactions. In this milieu, we demonstrated that (-)-catechin decreased the expression and secretion of proinflammatory cytokines, including interleukin (IL)-1β and IL-6. In conclusion, (-)-catechin is a candidate to ameliorate both intrinsic and extrinsic skin aging.
机译:在皮肤老化期间产生反应性氧物质(ROS),包括内在(年代老化)和外部老化(光学衰老)。因此,抑制ROS生成的抗氧化剂可以延缓皮肤衰老。在这项研究中,我们评估了( - ) - 酚醛化合物的潜在抗皮肤衰老效应从Ulmus Davidiana Var的根吠声中分离的潜在抗表扬效应。 japonica。我们优先考虑了分离株免于皮肤细胞外基质的降解的可能预防效果。在分离物中,( - ) - 儿茶素抑制了胶原酶MMP-1的活性,并逆转了正常人体皮肤成纤维细胞中肿瘤坏死因子-α(TNF-α)诱导的胶原蛋白的降解。通过抑制肿瘤坏死因子-α-诱导的ROS诱导的ROS和活性丝裂解蛋白激酶,蛋白激酶B(AKT)和环氧氧基酶-2(COX-2)的抑制肿瘤坏死因子-α-诱导的作用机制。(COX-2) 。促炎细胞因子上调炎症反应,最终促进与衰老相关的反应。在这个Milieu中,我们证明( - ) - 儿茶素减少了促炎细胞因子的表达和分泌,包括白细胞介素(IL)-1β和IL-6。总之,( - ) - 儿茶素是改善内在和外在皮肤老化的候选者。

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