Nondenatured soy extracts reduce UVB-induced skin damage via multiple mechanisms

Nannan Chen1, Richard Scarpa, Li Zhang

  • 1The Johnson & Johnson Skin Research Center, Consumer Products Worldwide, Johnson & Johnson Consumer Companies, Inc., Skillman, NJ, USA.

Insights

Topical soy extracts significantly reduced UVB-induced skin damage and DNA alterations in mice. This suggests soy may offer a natural approach to prevent skin cancer development and progression.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Cancer Research

Background:

  • Ultraviolet (UV) irradiation causes DNA damage, inflammation, and immunosuppression, contributing to skin cancer development.
  • Nondenatured soy extracts have previously shown potential in reducing skin tumor incidence and progression in mice.

Purpose of the Study:

  • To investigate the protective mechanisms of nondenatured soy extracts against UVB-induced skin damage.
  • To evaluate soy's impact on DNA repair, inflammation, and angiogenesis in the context of UV-induced skin carcinogenesis.

Main Methods:

  • Mice were pretreated topically with nondenatured soy extracts before UVB irradiation.
  • Analysis included measuring Thymine-Thymine (TT) dimer formation, checkpoint kinase-1 (Chk1) activation, cyclo-oxygenase-2 (COX-2) expression, and prostaglandin E2 secretion.
  • In vitro assays assessed endothelial tube formation to evaluate anti-angiogenic potential.

Main Results:

  • Soy pretreatment reduced UVB-induced TT dimer formation and COX-2 expression in mouse skin.
  • In vitro studies indicated enhanced Chk1 activation, suggesting improved DNA repair capacity.
  • Soy extracts inhibited UVB-induced inflammatory markers and endothelial tube formation, indicating anti-inflammatory and anti-angiogenic effects.

Conclusions:

  • Nondenatured soy extracts mitigate UVB-induced skin damage through multiple mechanisms, including enhanced DNA repair and reduced inflammation.
  • Topical soy application may offer a preventative strategy against skin cancer initiation and progression by combating UV-induced cellular damage and angiogenesis.

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