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Oral administration of collagen peptide in SKH-1 mice suppress UVB-induced wrinkle and dehydration through MAPK and MAPKK signaling pathways, in vitro and in vivo evidence

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Abstract

Skin aging is induced by exposure to extrinsic factors, causing various diseases and adversely affecting aesthetics. Studies have suggested that as the quality of life improves, demand for beauty and nutritional cosmetics increases. Here, the protective effects of collagen peptide against UV-induced skin damage were evaluated in vitro and in vivo. Collagen peptide inhibited water loss and UVB irradiation-induced HA degradation in the skin of SKH-1 mice. Additionally, collagen peptide dose-dependently inhibited UVB-induced wrinkle formation, epidermal thickness, and elastase activity. These results suggest that collagen peptide regulates collagen degradation through the MAPK and MAPKK pathway. In addition, collagen peptide administration did not affect changes in weight of the liver, spleen, and kidney, or enzymatic indicators of liver damage. Taken together, oral administration of collagen peptide improved the effects of UV-induced skin aging without toxicity. Therefore, this study supports the development of collagen peptide for skin aging prevention in nutricosmetic products.

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Acknowledgements

This work was supported by Korea Institute of Planning and Evaluation for Technology in Food, Agriculture and Forestry (IPET) through Technology Commercialization Support Program funded by Ministry of Agriculture, Food and Rural Affairs (MAFRA) (grant number: 821018-3) and supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (No. 2020R1C1C1004670).

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Authors and Affiliations

  1. Department of Food Science & Biotechnology, Sejong University, Seoul, 05006, Republic of Korea

    Cheol Hyeon Cho, Woo-Jin Sim & Tae-Gyu Lim

  2. Department of Food Science & Biotechnology, and Carbohydrate Bioproduct Research Center, Sejong University, Seoul, 05006, Republic of Korea

    Wonchul Lim & Tae-Gyu Lim

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  1. Cheol Hyeon Cho
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Supplementary Information

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10068_2023_1362_MOESM1_ESM.tif

Supplementary file1 (TIF 18341 KB)—Fig. S1 Molecular weight of collagen peptide. The molecular weight of collagen peptide was determined by SDS-PAGE and Coomassie blue staining.

10068_2023_1362_MOESM2_ESM.tif

Supplementary file2 (TIF 18341 KB)—Fig. S2 Oral ingestion of collagen peptide and HA did not appeared toxicity in mice. (a) body weight and (b) food intake were measured after 14 weeks of oral administration of collagen peptide and HA. Hepatotoxicity indicators, (c) AST and (d) ALT levels, (e) Liver, (f) spleen and (g) kidney weight was measured after 14 weeks of oral administration of collagen-peptide and HA. Sixty mice were randomly divided into 6 groups (n=10)

10068_2023_1362_MOESM3_ESM.tif

Supplementary file3 (TIF 18008 KB)—Fig. S3 Histological analysis after oral intake of collagen peptides and HA in mice skin. (a) The amount of collagen content in SKH-1 skin was measured using Massons’s trichrome staining. (b) Skin tissue stained in SKH-1 mice was measured using hematoxylin and eosin (H&E). (c) MMP-1 was stained in the skin tissue via immunohistochemistry staining. The area 2× magnified is indicated by a red line. Sixty mice were randomly divided into 6 groups (n=10). (Black or red scale bars of the tissue image is 100 or 50 μm, respectively.)

10068_2023_1362_MOESM4_ESM.tif

Supplementary file4 (TIF 19833 KB)—Fig. S4 Cytotoxicity of collagen peptide and HA in HaCaT and HDF cells. (a, e) Collagen peptide treatment cell viability in HDF cells. (b) HA treatment cell viability in HDF cells. (c, f) Collagen peptide treatment cell viability in HaCaT cells. (d) HA treatment cell viability in HaCaT cells. (Scale bar of the cell image is 400 μm.)

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Cho, C.H., Lim, W., Sim, WJ. et al. Oral administration of collagen peptide in SKH-1 mice suppress UVB-induced wrinkle and dehydration through MAPK and MAPKK signaling pathways, in vitro and in vivo evidence. Food Sci Biotechnol 33, 955–967 (2024). https://doi.org/10.1007/s10068-023-01362-6

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