The Extract from Acidosasa longiligula Alleviates in vitro UV-Induced Skin Cell Damage via Positive Regulation of Thioredoxin 1

• Published in: Clinical interventions in aging Vol. 15; pp. 897 - 905
• Main Authors: Huang, Jin-Wen, Xu, Qiu-Yun, Lin, Min, Cheng, Bo, Ji, Chao
• Format: Journal Article
• Language: English
• Published: New Zealand Taylor & Francis Ltd 01.01.2020; Dove; Dove Medical Press
• Subjects: acidosasa longiligula; Antibodies; Apoptosis; Apoptosis - drug effects; bamboo extract (bex); Deoxyribonucleic acid; DNA; Humans; Keratinocytes - metabolism; Metabolism; nf-κb pathway; Original Research; Oxidative stress; Plant Extracts - pharmacology; Poaceae; Proteins; Radiation-Protective Agents - pharmacology; Reactive Oxygen Species - metabolism; Skin; Skin - drug effects; Skin diseases; thioredoxin (txn); ultraviolet (uv) radiation; Ultraviolet radiation; Ultraviolet Rays - adverse effects; United States > US; China; UV radiation; ultraviolet radiation; BEX; thioredoxin; Acidosasa longiligula; NF-κB pathway; TXN; bamboo extract
• ISSN: 1178-1998; 1176-9092; 1178-1998
• DOI: 10.2147/CIA.S239920

Skin, as the outermost organ, is exposed to a wide range of environmental risk factors including ultraviolet (UV) and all kinds of pollutants. Excessive UV exposure contributes to many disorders, such as photoaging, skin inflammation, and carcinogenesis. To determine the effects of bamboo extract (BEX) from our local plant, , on UV-irritated human skin, we conducted a variety of studies, including Western blot, apoptosis assays, reactive oxygen species (ROS) detection, and thioredoxin (TXN) and thioredoxin reductase (TXNRD) activity assays in primary skin keratinocytes. We first determined that BEX protects human skin keratinocytes against UV radiation-induced apoptosis and ROS production. UV radiation can robustly impair TXN and TXNRD activity which can, in turn, be significantly rescued by BEX treatment. Moreover, BEX regulates TXN1 levels in primary skin keratinocytes and TXN1 is proved to be required for the protective function of BEX. Last, we found that the NF-κB/p65 pathway mediates the protective function of BEX against UV. Collectively, our work delineates the beneficial role of BEX in UV-induced skin cell damage and provides a novel therapeutic reagent to prevent or alleviate the progress of photoaging and other UV-provoked skin diseases.