Abstract
Objective: This study aimed to observe the effects of Achatina fulica mucus (AFM) on ultraviolet B (UVB)-induced fibroblast photoaging by assessing monocyte chemotactic protein (MCP)-1, vascular endothelial growth factor (VEGF), matrix metalloproteinases (MMP)-3, and MMP-12 mRNA expressions.
 Methods: Cell cultures of normal human dermal fibroblasts (NHDFs) were divided into six groups: Group 1 was normal fibroblasts without UVB irradiation as normal control and Groups 2–5 consisted of 100 mJ/cm2 UVB-induced aged fibroblasts. Group 2 had no treatment as negative control, Group 3 was treated by platelet-rich plasma 10% as positive control group, and Groups 4–6 were treated by various concentrations of AFM (3.9 μl, 15.625 μl, and 62.5 μl). The MCP-1, VEGF, MMP-3, and MMP-12 mRNA expressions in the different NHDF groups were assessed by quantitative polymerase chain reaction.
 Results: The mRNA expressions of MCP-1, VEGF, MMP-3, and MMP-12 in the AFM group compared to the UVB group decreased 8, 5, 5, and 4 folds, respectively. AF62 exhibited the highest improvement among the other AFM-treated groups.
 Conclusion: AFM treatment attenuates UVB-induced fibroblasts photoaging by reducing inflammation, angiogenesis, and matrix metalloproteinases.
Highlights
The main external factor for skin aging is ultraviolet (UV) radiation, ultraviolet B (UVB) (290–320 nm)
The mRNA expressions of monocyte chemotactic protein (MCP)-1, vascular endothelial growth factor (VEGF), matrix metalloproteinases (MMP)-3, and MMP-12 in the Achatina fulica mucus (AFM) group compared to the UVB group decreased 8, 5, 5, and 4 folds, respectively
AFM treatment attenuates UVB-induced fibroblasts photoaging by reducing inflammation, angiogenesis, and matrix metalloproteinases
Summary
The main external factor for skin aging is ultraviolet (UV) radiation, UVB (290–320 nm). UVB is responsible for skin damage called photoaging which is represented by crinkle, lose elasticity, frailty, rough skin texture, and teleangiectasies [2] This condition occurs because UVB triggers inflammation and degradation of the extracellular matrix such as collagen and elastin [3]. MCP-1 is the most prominent chemokines of the senescence-associated secretory phenotype (SASP) that expressed and released by fibroblasts and endothelial cells, leading to inflammation and vascular changes in the skin. This vascular changes managed by angiogenic factors as well as vascular endothelial growth factor (VEGF) [4]. The MMP responsible for collagen degradation is MMP-3 while for elastin degradation, it is MMP-12 [5]
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