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

Biomed Pharmacother. 2022 Nov:155:113727. doi: 10.1016/j.biopha.2022.113727. Epub 2022 Sep 23.

Abstract

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 electrospinning 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. Immunofluorescence experiments also showed that CPD could reduce the fluorescence intensity of Caspase-3 and TNF-α. These results suggest that CPD may be a successful healing agent that provides reinforcement against UVA-induced oxidative and irritating skin compensation.

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

MeSH terms

  • Antioxidants / metabolism
  • Antioxidants / pharmacology
  • Apoptosis
  • Caspase 3 / metabolism
  • Humans
  • Inflammation / metabolism
  • Inflammation / prevention & control
  • Keratinocytes / metabolism
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-E2-Related Factor 2* / metabolism
  • Nanofibers*
  • Oxidative Stress
  • Reactive Oxygen Species / metabolism
  • Superoxide Dismutase / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Ultraviolet Rays / adverse effects

Substances

  • Antioxidants
  • Caspase 3
  • NF-E2-Related Factor 2
  • Reactive Oxygen Species
  • Superoxide Dismutase
  • taxifolin
  • Tumor Necrosis Factor-alpha
  • Mitogen-Activated Protein Kinases