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Heat-Killed Lacticaseibacillus paracasei Ameliorated UVB-Induced Oxidative Damage and Photoaging and Its Underlying Mechanisms
Ultraviolet B (UVB) radiation is a major environmental causative factor of skin oxidative damage and photoaging. Lacticaseibacillus paracasei is a well-known probiotic strain that can regulate skin health. The present study investigated the effects of heat-killed Lacticaseibacillus paracasei (PL) on...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9598452/ https://www.ncbi.nlm.nih.gov/pubmed/36290598 http://dx.doi.org/10.3390/antiox11101875 |
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author | Xu, Jing Zhang, Xiaofang Song, Yan Zheng, Bin Wen, Zhengshun Gong, Miao Meng, Lingting |
author_facet | Xu, Jing Zhang, Xiaofang Song, Yan Zheng, Bin Wen, Zhengshun Gong, Miao Meng, Lingting |
author_sort | Xu, Jing |
collection | PubMed |
description | Ultraviolet B (UVB) radiation is a major environmental causative factor of skin oxidative damage and photoaging. Lacticaseibacillus paracasei is a well-known probiotic strain that can regulate skin health. The present study investigated the effects of heat-killed Lacticaseibacillus paracasei (PL) on UVB linked oxidative damage and photoaging in skin cells (Normal human dermal fibroblast (NHDF) cells and B16F10 murine melanoma cells). Results demonstrated that: (1) PL prevented UVB-induced cytotoxicity relating to decreased DNA damage in NHDF and B16F10 cells; (2) PL alleviated UVB-induced oxidative damage through increasing GSH content, as well as antioxidant enzyme activities and mRNA levels (except MnSOD activity and mRNA levels as well as CAT mRNA level) relating to the activation of Sirt1/PGC-1α/Nrf2 signaling in NHDF cells; (3) PL attenuated UVB-induced photoaging was noticed with a decrease in the percentage of SA-β-gal positive cells in NHDF cells model. Moreover, PL attenuated UVB-induced photoaging through exerting an anti-wrinkling effect by enhancing the type I collagen level relating to the inhibition (JNK, p38)/(c-Fos, c-Jun) of signaling in NHDF cells, and exerting an anti-melanogenic effect by suppressing tyrosinase and TYRP-1 activity and/or expressions relating to the inhibition of PKA/CREB/MITF signaling in B16F10 cells. In conclusion, PL could ameliorate UVB-induced oxidative damage and photoaging. Therefore, PL may be a potential antioxidant and anti-photoaging active ingredient for the cosmetic industry. |
format | Online Article Text |
id | pubmed-9598452 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-95984522022-10-27 Heat-Killed Lacticaseibacillus paracasei Ameliorated UVB-Induced Oxidative Damage and Photoaging and Its Underlying Mechanisms Xu, Jing Zhang, Xiaofang Song, Yan Zheng, Bin Wen, Zhengshun Gong, Miao Meng, Lingting Antioxidants (Basel) Article Ultraviolet B (UVB) radiation is a major environmental causative factor of skin oxidative damage and photoaging. Lacticaseibacillus paracasei is a well-known probiotic strain that can regulate skin health. The present study investigated the effects of heat-killed Lacticaseibacillus paracasei (PL) on UVB linked oxidative damage and photoaging in skin cells (Normal human dermal fibroblast (NHDF) cells and B16F10 murine melanoma cells). Results demonstrated that: (1) PL prevented UVB-induced cytotoxicity relating to decreased DNA damage in NHDF and B16F10 cells; (2) PL alleviated UVB-induced oxidative damage through increasing GSH content, as well as antioxidant enzyme activities and mRNA levels (except MnSOD activity and mRNA levels as well as CAT mRNA level) relating to the activation of Sirt1/PGC-1α/Nrf2 signaling in NHDF cells; (3) PL attenuated UVB-induced photoaging was noticed with a decrease in the percentage of SA-β-gal positive cells in NHDF cells model. Moreover, PL attenuated UVB-induced photoaging through exerting an anti-wrinkling effect by enhancing the type I collagen level relating to the inhibition (JNK, p38)/(c-Fos, c-Jun) of signaling in NHDF cells, and exerting an anti-melanogenic effect by suppressing tyrosinase and TYRP-1 activity and/or expressions relating to the inhibition of PKA/CREB/MITF signaling in B16F10 cells. In conclusion, PL could ameliorate UVB-induced oxidative damage and photoaging. Therefore, PL may be a potential antioxidant and anti-photoaging active ingredient for the cosmetic industry. MDPI 2022-09-21 /pmc/articles/PMC9598452/ /pubmed/36290598 http://dx.doi.org/10.3390/antiox11101875 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Xu, Jing Zhang, Xiaofang Song, Yan Zheng, Bin Wen, Zhengshun Gong, Miao Meng, Lingting Heat-Killed Lacticaseibacillus paracasei Ameliorated UVB-Induced Oxidative Damage and Photoaging and Its Underlying Mechanisms |
title | Heat-Killed Lacticaseibacillus paracasei Ameliorated UVB-Induced Oxidative Damage and Photoaging and Its Underlying Mechanisms |
title_full | Heat-Killed Lacticaseibacillus paracasei Ameliorated UVB-Induced Oxidative Damage and Photoaging and Its Underlying Mechanisms |
title_fullStr | Heat-Killed Lacticaseibacillus paracasei Ameliorated UVB-Induced Oxidative Damage and Photoaging and Its Underlying Mechanisms |
title_full_unstemmed | Heat-Killed Lacticaseibacillus paracasei Ameliorated UVB-Induced Oxidative Damage and Photoaging and Its Underlying Mechanisms |
title_short | Heat-Killed Lacticaseibacillus paracasei Ameliorated UVB-Induced Oxidative Damage and Photoaging and Its Underlying Mechanisms |
title_sort | heat-killed lacticaseibacillus paracasei ameliorated uvb-induced oxidative damage and photoaging and its underlying mechanisms |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9598452/ https://www.ncbi.nlm.nih.gov/pubmed/36290598 http://dx.doi.org/10.3390/antiox11101875 |
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