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甲基异鼠李素和甲基异鼠李素-3-O-β-D-吡喃葡萄糖苷对肿瘤坏死因子-α诱导的人皮肤成纤维细胞炎症的保护作用。

Protective effects of methylnissolin and methylnissolin-3-O-β-d-glucopyranoside on TNF-α-induced inflammation in human dermal fibroblasts.

作者信息

Choi Yea Jung, Wu Xiaohua, Lee Sullim, Pyo Jae Sung, Cho Jaejin, Cao Shugeng, Kang Ki Sung

机构信息

Department of Preventive Medicine, College of Korean Medicine, Gachon University, Seongnam 13120, Republic of Korea.

Department of Pharmaceutical Sciences, Daniel K. Inouye College of Pharmacy, University of Hawaii at Hilo, Hilo, HI 96720, United States.

出版信息

Toxicol In Vitro. 2025 Apr;104:106005. doi: 10.1016/j.tiv.2024.106005. Epub 2024 Dec 31.

Abstract

Methylnissolin-3-O-β-d-glucopyranoside (MNG) and methylnissolin (MN) are pterocarpan derivatives that are found in plants, such as Astragalus membranaceus. There are limited existing studies on the potential health benefits of MNG, and currently there is no evidence to suggest that MNG has any impact on skin-aging. Tumor necrosis factor-alpha (TNF-α) plays a significant role in skin aging by promoting chronic inflammation, damaging skin cells, and impairing the skin's natural repair mechanisms. Targeting TNF-α or its downstream signaling pathways may be a promising strategy for preventing or reversing skin-aging. We tested the effect of MNG and MN on skin-aging by inducing cell inflammation and oxidative stress with TNF-α in HDFs. MNG and MN significantly reduced the TNF-α-induced secretion of matrix metalloproteinase-1 (MMP-1). However, MNG has more beneficial compound for oral administration than MN in pharmacokinetics analysis. The mechanism underlying the anti-skin-aging effect of MNG is related to the suppression of TNF-α-induced reactive oxygen species (ROS) generation and mitogen-activated protein kinase (MAPKs) phosphorylation. Our results suggest that MNG is a potential candidate for preventing skin-aging induced by TNF-α.

摘要

甲基异鼠李素-3-O-β-D-吡喃葡萄糖苷(MNG)和甲基异鼠李素(MN)是在诸如黄芪等植物中发现的紫檀烷衍生物。关于MNG潜在健康益处的现有研究有限,目前没有证据表明MNG对皮肤衰老有任何影响。肿瘤坏死因子-α(TNF-α)通过促进慢性炎症、损害皮肤细胞和破坏皮肤的自然修复机制,在皮肤衰老中起重要作用。靶向TNF-α或其下游信号通路可能是预防或逆转皮肤衰老的一种有前景的策略。我们通过用TNF-α在人皮肤成纤维细胞(HDFs)中诱导细胞炎症和氧化应激,测试了MNG和MN对皮肤衰老的影响。MNG和MN显著降低了TNF-α诱导的基质金属蛋白酶-1(MMP-1)的分泌。然而,在药代动力学分析中,MNG作为口服给药的化合物比MN更具优势。MNG抗皮肤衰老作用的潜在机制与抑制TNF-α诱导的活性氧(ROS)生成和丝裂原活化蛋白激酶(MAPKs)磷酸化有关。我们的结果表明,MNG是预防TNF-α诱导的皮肤衰老的潜在候选物。

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