4.7 Article

Dihydroquercetin composite nanofibrous membrane prevents UVA radiation-mediated inflammation, apoptosis and oxidative stress by modulating MAPKs/Nrf2 signaling in human epidermal keratinocytes

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 155, Issue -, Pages -

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2022.113727

Keywords

Dihydroquercetin composite nanofibrous; membrane; UVA-radiation; Photodamage; Oxidative damage; Inflammation; Apoptosis

Funding

  1. Science and Technology Develop-ment Plan Project of the Science and Technology Department of Jilin Province
  2. [20210203130SF]

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The study found that Dihydroquercetin composite nanofiber membrane (CPD) can reduce skin inflammation and photodamage caused by UVA radiation by enhancing the activity of antioxidant enzymes and reducing ROS expression. CPD also prevents inflammation, apoptosis, and oxidative stress induced by MAPK/Nrf2 signaling pathway. Immunofluorescence experiments showed that CPD can reduce the fluorescence intensity of Caspase-3 and TNF-alpha.
Exposure to ultraviolet (UV) radiation is a key cause of skin inflammation and photodamage in the environment. Dihydroquercetin composite nanofiber membrane (CPD) is a nano-scale membrane cloth prepared by electro-spinning technology. The results in this study showed that CPD could enhance the activities of endogenous antioxidant enzymes such as SOD and GSH-Px induced by UVA radiation, and reduce the overexpression of ROS. MAPKs/Nrf2 signaling is associated with inflammation, apoptosis and oxidative stress. Compared with control HaCaT cells, we found that CPD pretreatment prevents MAPK (p-ERK, p-JNK, and p-P38)/Nrf2-induced inflammation, apoptosis, and oxidative stress signaling during UVA exposure pathway overexpression. Immu-nofluorescence experiments also showed that CPD could reduce the fluorescence intensity of Caspase-3 and TNF-alpha. These results suggest that CPD may be a successful healing agent that provides reinforcement against UVA-induced oxidative and irritating skin compensation.

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