Abstract
Background Nanofat can protect against ultraviolet B- (UVB-) induced damage in nude mice. Fat extract (FE) is a cell-free fraction isolated from nanofat that is enriched with a variety of growth factors. Objective To determine whether FE can protect against UVB-induced photoaging in cultured dermal fibroblasts and in nude mice. Method For the in vitro study, human dermal skin fibroblasts were pretreated with FE 24 h prior to UVB irradiation. Generation of reactive oxygen species (ROS) was analyzed immediately following irradiation, while cell cycle analysis was performed 24 h after UVB irradiation. Senescence-associated β-galactosidase (SA-β-gal) expression, cell proliferation, and expression of glutathione peroxidase 1 (GPX-1), catalase, superoxide dismutase-1 (SOD-1), SOD-2, and collagen type 1 (COL-1) were investigated 72 h after UVB irradiation. For the in vivo study, the dorsal skin of nude mice was irradiated with UVB and mice were then treated with FE for 8 weeks. The thickness of the dermis, capillary density, and apoptotic cells in skin tissue sections were investigated after treatment. The expression of GPX-1, catalase, SOD-2, SOD-1, and COL-1 in the tissue was also measured. Result FE significantly increased cell proliferation and protected cells against UVB-induced cell death and cell cycle arrest. FE reduced ROS and the number of aged cells induced by UVB irradiation. FE promoted the expression of COL-1 and GPX-1 in cultured dermal fibroblasts. FE treatment of UVB-irradiated skin increased dermal thickness and capillary density, decreased the number of apoptotic cells, and promoted the expression of COL-1 and GPX-1. Conclusion FE protects human dermal fibroblasts and the skin of nude mice from UVB-induced photoaging through its antioxidant, antiapoptotic, and proangiogenic activities.
Highlights
The ultraviolet (UV) irradiation inherent to sun exposure is the main factor leading to skin aging, which is known as photoaging [1, 2]
To detect the effect of Fat extract (FE) on human skin fibroblasts, cell proliferation was measured after FE treatment either with or without UVB irradiation
Cell proliferation was significantly decreased after UVB irradiation, while FE
Summary
The ultraviolet (UV) irradiation inherent to sun exposure is the main factor leading to skin aging, which is known as photoaging [1, 2]. UVB irradiation can induce damage in dermal fibroblasts by producing reactive oxygen species (ROS), such as superoxide anion, hydroxyl free radicals, and hydrogen peroxide [4]; this results in decreased ECM production and remodeling [5,6,7]. Strategies for reducing the accumulation of intracellular ROS have been promoted to prevent UVB-induced cell death and protect skin from aging [8, 9]. To determine whether FE can protect against UVB-induced photoaging in cultured dermal fibroblasts and in nude mice. FE treatment of UVB-irradiated skin increased dermal thickness and capillary density, decreased the number of apoptotic cells, and promoted the expression of COL-1 and GPX-1. FE protects human dermal fibroblasts and the skin of nude mice from UVB-induced photoaging through its antioxidant, antiapoptotic, and proangiogenic activities
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