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人类皮肤成纤维细胞对空气污染的适应性反应及其在衰老中的潜在作用。

Adaptive responses to air pollution in human dermal fibroblasts and their potential roles in aging.

作者信息

Reynolds Wil J, Bowman Amy, Hanson Peter S, Critchley Adam, Griffiths Ben, Chavan Bhaven, Birch-Machin Mark A

机构信息

Dermatological Sciences, Translational and Clinical Research Institute Newcastle University Newcastle upon Tyne UK.

Mental Health Dementia and Neurodegeneration, Translational and Clinical Research Institute Newcastle University Newcastle upon Tyne UK.

出版信息

FASEB Bioadv. 2021 Jul 17;3(10):855-865. doi: 10.1096/fba.2021-00056. eCollection 2021 Oct.

Abstract

The damaging effects of air pollution on the skin are becoming increasingly researched and the outcomes of this research are now a major influence in the selection and development of protective ingredients for skincare formulations. However, extensive research has not yet been conducted into the specific cellular defense systems that are being affected after exposure to such pollutants. Research investigating the affected systems is integral to the development of suitable interventions that are capable of augmenting the systems most impacted by air pollutant exposure. The following studies involved exposing primary human dermal fibroblasts to different concentrations of particulate matter and analyzing its effects on mitochondrial complex activity, nuclear factor erythroid 2-related factor 2 localization using immunocytochemistry and protein expression of electron transport chain complex proteins, sirtuin-1 (SIRT1), and peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) using western blotting. Particulate matter-induced alterations in both mitochondrial complex protein and activity, indicating oxidative stress, which was also complimented by increased expression of antioxidant proteins GSTP1/2 and SOD2. Particulate matter also seemed to modify expression of the proteins SIRT1 and PGC-1α which are heavily involved in the regulation of mitochondrial biogenesis and energy metabolism. Given the reported results indicating that particulate matter induces damage through oxidative stress and has a profound effect on mitochondrial homeostasis, interventions involving targeted mitochondrial antioxidants may help to minimize the damaging downstream effects of pollutant-induced oxidative stress originating from the mitochondria.

摘要

空气污染对皮肤的损害作用正受到越来越多的研究,这些研究结果如今在护肤品配方中防护成分的选择和研发方面产生了重大影响。然而,对于暴露于此类污染物后受影响的特定细胞防御系统,尚未进行广泛研究。对受影响系统的研究对于开发合适的干预措施至关重要,这些干预措施能够增强受空气污染暴露影响最大的系统。以下研究包括将原代人皮肤成纤维细胞暴露于不同浓度的颗粒物,并使用免疫细胞化学分析其对线粒体复合物活性、核因子红细胞2相关因子2定位的影响,以及使用蛋白质印迹法分析电子传递链复合物蛋白、沉默调节蛋白1(SIRT1)和过氧化物酶体增殖物激活受体γ共激活因子1α(PGC-1α)的蛋白质表达。颗粒物诱导线粒体复合物蛋白和活性发生改变,表明存在氧化应激,抗氧化蛋白GSTP1/2和SOD2表达增加也证实了这一点。颗粒物似乎还会改变SIRT1和PGC-1α蛋白的表达,这两种蛋白在很大程度上参与线粒体生物合成和能量代谢的调节。鉴于报告结果表明颗粒物通过氧化应激诱导损伤并对线粒体稳态产生深远影响,涉及靶向线粒体抗氧化剂的干预措施可能有助于将源自线粒体的污染物诱导氧化应激的下游损害降至最低。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b22/8493965/45b110368541/FBA2-3-855-g002.jpg

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