Low-energy green light alleviates senescence-like phenotypes in a cell model of photoaging.

Abstract

Ultraviolet B (UVB) affects diverse pathways in skin cells, resulting in skin photoaging. Skin fibroblasts internalize and degrade elastin and collagen, playing prominent roles in photoaging. Green light is used in many fields of dermatology, but few studies have examined its role in photoaging. The present work aimed to assess low-energy green light for its effects in a previously proposed cell model of photoaging and to explore the possible anti-photoaging mechanism. The stress-induced premature senescence (SIPS) model was constructed via repeated treatment of MDFs with UVB. Senescence-like phenotypes were compared among normal, low-energy green light pretreatment and UVB groups, for example, cell morphological properties, senescence-associated β-galactosidase (SA-β-gal) amounts, extracellular matrix (ECM) biosynthesis and degradation, and autophagy. In comparison with the UVB group, the green light pretreatment group showed significantly decreased number of senescent mast cells and markedly declined signal intensity and amounts of SA-β-gal-positive cells. Furthermore, green light pretreatment directly affected ECM by increasing type I and type III collagen production and decreasing MMP-1 amounts. Moreover, changes in autophagy levels induced by green light pretreatment provided a potential mechanism underlying its anti-aging property. Low-energy green light pretreatment improves senescence-like phenotypes in vitro, indicating a possible application for anti-aging in clinic after future research has uncovered the potential mechanism.