Protective Effects of Polyvinylpyrrolidone-Wrapped Fullerene Against Nitric Oxide/Peroxynitrite-Induced Cellular Injury in Human Skin Keratinocytes
Protective Effects of Polyvinylpyrrolidone-Wrapped Fullerene Against Nitric Oxide/Peroxynitrite-Induced Cellular Injury in Human Skin Keratinocytes
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聚乙烯吡咯烷酮包裹的富勒烯对一氧化氮/过氧亚硝酸盐诱导的人皮肤角质形成细胞损伤的保护作用
DOI:
10.1166/jnn.2021.19279
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发表时间:
2021
影响因子:
--
通讯作者:
Hyodo Sayuri
中科院分区:
文献类型:
--
作者:
Saitoh Yasukazu;Tanaka Asuka;Hyodo Sayuri
Excess ultraviolet (UV) exposure accelerates skin inflammation, melanogenesis, wrinkle formation, photoaging, and carcinogenesis through oxidative stress and deoxyribonucleic acid damage. These deleterious effects to skin are closely associated with UV-induced reactive oxygen species (ROS) and reactive nitrogen species (RNS) produced via nitric oxide (NO·) generation. RNS are known to be responsible for various skin disorders, such as erythema, melanin production, reduced barrier function, and psoriasis. These skin disorders are major cosmetic problems; RNS control, in addition to ROS control, is important for maintaining healthy skin. In the present study, we investigated the cytoprotective effects of polyvinylpyrrolidone-entrapped fullerene (C60/PVP), a water-soluble ROS scavenger, against nitric oxide (NO·) and peroxynitrite (ONOO-)-induced human keratinocyte injuries. Protective effects of C60/PVP on NO·/ONOO--induced cellular damage and intracellular ONOO- generation were evaluated using a NO· donor S-nitroso-N-acetylpenicillamine (SNAP) in human skin epidermal HaCaT keratinocytes. Furthermore, the suppressive effect of C60/PVP on UVB-induced generation of intracellular ONOO- levels was also investigated. C60/PVP exerted suppressive effects on intracellular increases in NO·-induced ONOO- generation and subsequent cellular damage. Additionally, C60/PVP significantly decreased the UVB-induced generation of intracellular ONOO- levels. These findings suggest that C60/PVP could be useful as a cosmetics ingredient for prevention of skin injuries and/or dysfunction from NO·/ONOO--induced effects in human skin keratinocytes.