ADSCs inhibit photoaging- and photocarcinogenesis-related inflammatory responses and extracellular matrix degradation.

Background: Skin is a dynamic organ that maintains homeostasis and provides protection against environmental stimuli and pathogens. However, constant solar ultraviolet (UV) radiation can induce photoaging and photocarcinogenesis, thus reducing skin barrier function by altering skin at the cellular and structural levels. Adipose-derived stem cells (ADSCs) ameliorate signs of skin photoaging, but their antiphotoaging mechanism remains elusive. In this study, we explored the mechanism by which ADSCs improve skin photoaging. Methods: Female C57BL/6J mice were used as experimental subjects and were randomly divided into three groups. We used Western blot analysis, Real time-polymerase chain reaction, and immunofluorescence to analyze the expression of photoaging- and photocarcinogenesis-related inflammasomes, extracellular matrix components, and related factors. Results: The results showed that ADSCs reduced the UVB irradiation-mediated increase in MMP2, MMP13, phospho-NF-kappa B p65, Nlrp3, and VCAM-1 mRNA expression. The TGF-beta 2 expression trend was opposite that of the above genes. ADSCs ameliorated the downregulation of alpha 6 integrin, CD34, and collagen I by UVB irradiation. Simultaneously, ADSCs reduced the overexpression of COX2 and TNF-alpha induced by UVB irradiation. Conclusion: These results demonstrated that ADSCs could restore skin barrier function at the cellular and structural levels, enhance hair follicle stem cell (HFSCs) activity by regulating TGF-beta 2 and inhibit photoaging- and photocarcinogenesis-related inflammatory responses and extracellular matrix degradation.