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3-去氧胆酸查尔酮通过抑制激活蛋白-1 和核因子-κB 的 DNA 结合活性抑制肿瘤坏死因子-α诱导的人角质形成细胞基质金属蛋白酶-9 的表达。

3-Deoxysappanchalcone inhibits tumor necrosis factor-α-induced matrix metalloproteinase-9 expression in human keratinocytes through activated protein-1 inhibition and nuclear factor-kappa B DNA binding activity.

机构信息

Natural Product Chemistry Laboratory, College of Pharmacy, Ewha Womans University, Seoul, Korea.

出版信息

Biol Pharm Bull. 2011;34(6):890-3. doi: 10.1248/bpb.34.890.

Abstract

Tumor necrosis factor α (TNF-α), which is a primary cytokine responsible for inflammatory responses in skin, induces the synthesis of matrix metalloproteinase-9 (MMP-9), which causes skin aging. The protective effects of 3-deoxysappanchalcone against TNF-α-induced damage was investigated using human skin keratinocytes. The results showed that 3-deoxysappanchalcone inhibited MMP-9 expression at the protein and mRNA level, by blocking the activation of activator protein-1 (AP-1) and nuclear factor kappa B (NF-κB). Taken together, the inhibitory activity of 3-deoxysappanchalcone on MMP-9 expression and production in TNF-α-treated cells was found to be mediated by the suppression of AP-1 and NF-κB activation.

摘要

肿瘤坏死因子-α(TNF-α)是一种主要的细胞因子,负责皮肤的炎症反应,诱导基质金属蛋白酶-9(MMP-9)的合成,从而导致皮肤衰老。使用人皮肤角质形成细胞研究了 3-去氧萨潘亭酮对 TNF-α诱导损伤的保护作用。结果表明,3-去氧萨潘亭酮通过阻断激活蛋白-1(AP-1)和核因子 kappa B(NF-κB)的激活,抑制 MMP-9 在蛋白质和 mRNA 水平的表达。综上所述,发现 3-去氧萨潘亭酮对 TNF-α处理细胞中 MMP-9 表达和产生的抑制活性是通过抑制 AP-1 和 NF-κB 激活来介导的。

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