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.2024 Jul 9;10(15):e34321.
doi: 10.1016/j.heliyon.2024.e34321. eCollection 2024 Aug 15.

Synergistic delivery of hADSC-Exos and antioxidants has inhibitory effects on UVB-induced skin photoaging

Affiliations

Synergistic delivery of hADSC-Exos and antioxidants has inhibitory effects on UVB-induced skin photoaging

Yu Fu et al. Heliyon..

Abstract

Ultraviolet B (UVB) light exposure accelerates skin photoaging. Human adipose-derived stem cell exosomes (hADSC-Exos) and some antioxidants may have anti-photoaging effects. However, it is unknown whether the combination of hADSC-Exos and antioxidants plays a synergistic role in anti-photoaging. In cellular and 3D skin models, we showed that vitamin E (VE) and hADSC-Exos were optimal anti-photoaging combinations. In vivo, VE and hADSC-Exos increased skin tightening and elasticity in UVB-induced photoaging mice Combined treatment with VE and hADSC-Exos inhibited SIRT1/NF-κB pathway. These findings contribute to the understanding of hADSC-Exos in conjunction with other antioxidants, thereby providing valuable insights for the future pharmaceutical and cosmetic industries.

Keywords: Anti-Photoaging; Antioxidants; Skin rejuvenation; Synergistic delivery; hADSC-Exos.

© 2024 The Authors.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1
Fig. 1
Identification of the exosome from hADSC. a Morphology of hADSC. Scale bar = 100 μm b multiple differentiation potential of hADSC Scale bar = 100 μm. c Surface markers profiling of hADSC. The cells were highly positive for CD73, CD90, and CD105 and were negative for CD45 and HLA-DR. d. By TEM, purified hADSC-Exo exhibit cup-like morphologies. e Nanoparticle analysis of hADSC-Exo. f. The protein markers in hADSC and hADSC-Exos were analyzed by WB. hADSC expressed Calnexin and hADSC-Exo expressed CD81, CD63, and CD9. Full-length blots/gels are presented in Supplementary original image of the blotting.
Fig. 2
Fig. 2
hADSCs-Exo and antioxidants protected HaCaT cells from UVB. a Flow cytometric analysis of apoptotic cells in control group and UV group. b-c Images of senescence-associated SA-β-gal staining of proliferating and senescent HaCaT cells. Control group and UV group (b). hADSCs-Exo and antioxidants protected HaCaT cells from UVB-induced apoptosis in SA-β-gal staining (c). d The migratory properties of HaCaT cells were analyzed using the Transwell migration assay with Transwell filter chambers. e WB Western blot. In UV group, the level of COL17 downregulated and MMP3 levels upregulated by UVB. hADSC-Exo and five antioxidants transfection rescued the expression level of COL17 and MMP3 to different extents. Full-length blots/gels are presented in Supplementary original image of the blotting. Quantification of COL17 and MMP3, normalized to GAPDH levels, and values were plotted. Idebenone (IDE), chlorogenic acid (CGA), vitamin C (VC), VE, zinc (Zn). n = 3. Control, non-exposed HaCaT cells. UV, UVB-exposed HaCaT cells. IDE + EXO, hADSC-Exo and Idebenone-pretreated UVB-exposed HaCaT cells. CGA + EXO, hADSC-Exo and chlorogenic acid-pretreated UVB-exposed HaCaT cells. VC + EXO, hADSC-Exo and vitamin C-pretreated UVB-exposed HaCaT cells. VE + EXO, hADSC-Exo and vitamin E-pretreated UVB-exposed HaCaT cells. Zn + EXO, hADSC-Exo and zinc-pretreated UVB-exposed HaCaT cells. Differences in eight groups were assessed by Tukey's multiple comparison test one-way ANOVA, error bars represent S.E.M. Compared with control group, markered with *p < 0.05, **p < 0.01, ***p < 0.001. Compared with UV group, markered with #p < 0.05,##p < 0.01,###p < 0.001,####p < 0.0001.
Fig. 3
Fig. 3
hADSC-Exo and VE delivery to synergistically against the UVB-induced photoaging in HaCaT cells. a-d Flow cytometric analysis of apoptotic cells in each group. Representative flow cytometric plots (a). b-d Statistical analysis of the results of flow apoptosis experiments in each group. The percentage of live cells (b). The percentage of early apoptosis cells (c). The stacked bar graphs indicate the mean percentage of viable, early apoptotic, and late apoptotic cells (d). e-f CCK8 assay. CCK8 assay was carried out to measure the cell growth in 48 h (e). Cell survival was determined by the CCK8 assay at 12 h (f). g and i SA-β-gal staining. Senescent cells showed a blue staining (g). Statistics of senescence in shown (i). h and j Transwell migration assay. Transwell migration image in each group (h). Quantification of transwell migration assay data (j). k and l ROS. Representative graphs of flow cytometry analysis for ROS levels in HaCaT cells (k). Detection of ROS level in HaCaT cells by DCF fluorescence (l). n = 3. Control, non-exposed HaCaT cells. UV, UVB-exposed HaCaT cells. UV + VE, VE-pretreated UVB-exposed HaCaT cells. UV + EXO, hADSC-Exo-pretreated UVB-exposed HaCaT cells. UV + VE + EXO, hADSC-Exo and VE-pretreated UVB-exposed HaCaT cells. Differences in five groups were assessed by Tukey's multiple comparison test one-way ANOVA, error bars represent S.E.M. Compared with control group, markered with *p < 0.05, **p < 0.01, ***p < 0.001. Compared with UV group, markered with #p < 0.05,##p < 0.01,###p < 0.001,####p < 0.0001. Compared with UV + EXO group, markered with $p < 0.05,$$p < 0.01,$$$p < 0.001,$$$$p < 0.0001.
Fig. 4
Fig. 4
hADSC-Exo and VE delivery to synergistically against the UVB-induced photoaging in 3D skin model. a-c HE staining of 3D skin model. Representative images in 3D skin model constructs. Stratum Basale (SB), Stratum Corneum (SC), Stratum Granulosum (SG), Stratum Spinosum (SS). (a). Analysis of the thickness of the epidermal layer of 3D skin model in HE staining sections (b). Thickness quantifications of the stratum epidermis (c). d-e Masson staining. Representative images in collagen deposition (blue, d). Quantification of 3D skin model for fibrosis with representative Masson trichrome image (e). f and i Representative photographs of TNF-α, immunostaining. Scale bar = 50 μm (f). Quantitative analysis of TNF-α (i). g and j Representative photographs of COL-17, immunostaining. Scale bar = 50 μm (g). Quantitative analysis of COL-17 (j). h and k Representative photographs of MMP3, immunostaining. Scale bar = 50 μm (h). Quantitative analysis of MMP3 (k). Control, non-exposed 3D skin model. UV, UVB-exposed 3D skin model. UV + VE, VE-pretreated UVB-exposed 3D skin model. UV + EXO, hADSC-Exo-pretreated UVB-exposed 3D skin model. UV + VE + EXO, hADSC-Exo and VE-pretreated UVB-exposed 3D skin model. Differences in five groups were assessed by Tukey's multiple comparison test one-way ANOVA, error bars represent S.E.M. Compared with control group, markered with *p < 0.05, **p < 0.01, ***p < 0.001. Compared with UV group, markered with #p < 0.05,##p < 0.01,###p < 0.001,####p < 0.0001.
Fig. 5
Fig. 5
hADSC-Exo and VE delivery to synergistically against the UVB-induced photoaging in photoaged mouse model. a Schematic flowchart of the experiment of UVB-exposed and shaved in photoaged mouse model. b The gross appearances of skin damaged by photoaging in each group. Mice were randomly grouped. Six animals were in each group. c and e HE staining of photoaged mouse model. Representative images in photoaged mouse model constructs (c). Thickness quantifications of the stratum epidermis of photoaged mouse model in HE staining sections (e). d and f Masson staining. Representative images in collagen deposition (blue, d). Quantification of photoaged mouse model for fibrosis with representative Masson trichrome image (f). g The changes of skin moisture content of the photoaged mouse model. h and k Representative photographs of TNF-α, immunostaining. Scale bar = 50 μm (h). Quantitative analysis of TNF-α (k). i and l Representative photographs of COL-17, immunostaining. Scale bar = 50 μm (i). Quantitative analysis of COL-17 (l). j and m Representative photographs of MMP3, immunostaining. Scale bar = 50 μm (j). Quantitative analysis of MMP3 (m). Control, non-exposed photoaged mouse skin. UV, UVB-exposed photoaged mouse skin. UV + VE, VE-pretreated UVB-exposed photoaged mouse skin. UV + EXO, hADSC-Exo-pretreated UVB-exposed photoaged mouse skin. UV + VE + EXO, hADSC-Exo and VE-pretreated UVB-exposed photoaged mouse skin. Differences in five groups were assessed by Tukey's multiple comparison test one-way ANOVA, error bars represent S.E.M. Compared with control group, markered with *p < 0.05, **p < 0.01, ***p < 0.001. Compared with UV group, markered with #p < 0.05,##p < 0.01,###p < 0.001,####p < 0.0001. Three mice were randomly selected from each group for histological examination.
Fig. 6
Fig. 6
Integrated bioinformatics analysis to identify anti-skin photoaging protein in hADSC-Exo. a The CTD analysis between potential key genes and diseases. b The up panel is a schematic representation of human inflammation antibody array containing 40 inflammation antibodies. c The color of the bubble indicates whether the pathway was upregulated (red) or no difference (gray) and the size of the bubble indicates to the degree of regulation. IL-6 is the most affected among the up-regulated inflammation factors after UVB exposure. d Heat map of the inflammatory cytokines. e UVB actives the signal pathway of related inflammatory factors. f VE modulated the IL-6 to alleviate inflammation. g Wayne diagram displaying the hub photoaging proteins in hADSC-Exo. h Photoaging-related protein abundance identified by mass spectrometry in the hADSC-Exo. i STRING network analysis of the photoaging-related protein interaction network.
Fig. 7
Fig. 7
The anti-skin photoaging function of hADSC exosomal SFN via a NF-κB signaling pathway is regulated by SIRT1. a and b Representative WB image of SIRT1, p-p65, p65 and IL-6 in each group (a). Quantitative analysis (b). c and d Representative WB image of SIRT1 after SFN overexpressed in HaCaT cells. Full-length blots/gels are presented in Supplementary original image of the blotting. WB Quantitative analysis and IL-6 quantification was performed by qPCR (d). e Schematic illustration of the role of hADSC-Exo and VE on protecting skin photoaging. n = 3. Control, non-exposed HaCaT cells. UV, UVB-exposed HaCaT cells. UV + VE, VE-pretreated UVB-exposed HaCaT cells. UV + EXO, hADSC-Exo-pretreated UVB-exposed HaCaT cells. UV + VE + EXO, hADSC-Exo and VE-pretreated UVB-exposed HaCaT cells. Differences in five groups were assessed by Tukey's multiple comparison test one-way ANOVA, error bars represent S.E.M. Compared with control group, markered with *p < 0.05, **p < 0.01, ***p < 0.001. Compared with UV group, markered with #p < 0.05,##p < 0.01,###p < 0.001,####p < 0.0001.
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References

    1. Lorz L.R., et al. Anti-wrinkling and anti-melanogenic effect of pradosia mutisii methanol extract. Int. J. Mol. Sci. 2019;20(5):1043. - PMC - PubMed
    1. Passeron T., et al. Photoprotection according to skin phototype and dermatoses: practical recommendations from an expert panel. J. Eur. Acad. Dermatol. Venereol. 2021;35(7):1460–1469. - PMC - PubMed
    1. Rachmin I., et al. Topical treatment strategies to manipulate human skin pigmentation. Adv. Drug Deliv. Rev. 2020;153:65–71. - PMC - PubMed
    1. Zou X., et al. Multi-omics analysis of an in vitro photoaging model and protective effect of umbilical cord mesenchymal stem cell-conditioned medium. Stem Cell Res. Ther. 2022;13(1):435. - PMC - PubMed
    1. Zhang Y., et al. Circ_0011129 encapsulated by the small extracellular vesicles derived from human stem cells ameliorate skin photoaging. Int. J. Mol. Sci. 2022;23(23) - PMC - PubMed

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