D. Lelièvre , F. Canivet , F. Thillou , C. Tricaud , C. Le Floc'h , F. Bernerd
{"title":"利用重建皮肤模型评估三种不同SPF值的防晒产品对DNA损伤和细胞改变的光保护作用","authors":"D. Lelièvre , F. Canivet , F. Thillou , C. Tricaud , C. Le Floc'h , F. Bernerd","doi":"10.1016/j.jpap.2023.100213","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><p>Both UVB and UVA rays induce biological damages in the epidermis and the dermis that contribute to photo-carcinogenesis and photoaging. In the present study, the photoprotective effect of 2 ISO standard sunscreens, P3 (Sun Protection Factor [SPF]15) and P6 (SPF40) and of an SPF50+ labeled commercial sunscreen product was tested in reconstructed skin tissues exposed to increasing doses of UV Solar Simulated Radiation (UV-SSR). UV-induced damages were evaluated using several biological markers, including DNA lesions in the presence or absence of sunscreen protection.</p></div><div><h3>Method</h3><p>T-Skin™ model samples (EPISKIN), composed of a fibroblast-populated dermal equivalent and a fully differentiated epidermis, were protected with the test sunscreens (1.3 mg/cm² topically applied on molded polymethyl methacrylate plate) before being exposed to increasing UV doses (0 – 2.5 – 5 - 25 – 40 J/cm²). Twenty-four hours after exposure, tissues with and without sunscreen protection, were analyzed for skin viability and morphology, DNA lesions (cyclobutane pyrimidine dimer) and inflammatory mediator quantification. Results were compared to untreated exposed tissues using a Wilcoxon non-parametric test.</p></div><div><h3>Results</h3><p>For untreated tissues, UV-SSR exposure induced a dose-dependent decrease in epidermal and dermal viabilities, an increase in release of proinflammatory cytokines and matrix metalloproteinases and were associated with morphological damages at doses as low as 5 J/cm<sup>2</sup>. DNA lesions were even detected at the lowest dose of 2.5 J/cm<sup>2</sup>, and their number increased with the UV-SSR dose. In the samples protected with sunscreens, these abnormalities were partially or totally prevented with P6 providing a better protection compared to P3, and the SPF50+ sunscreen showing a trend for better protection than P6, for example against DNA damage.</p></div><div><h3>Conclusions</h3><p>This study demonstrates that photoprotective effects of different sunscreens can be discriminated and ranked on reconstructed skin tissues (T-Skin™ model) exposed to UV-SSR. Showing significant differences between the reference products P3 and P6 in line with their respective SPF values, such study allows the evaluation of epidermal and dermal damages at the tissue, cellular and molecular levels. It thus opens the way to a new model of integrated assessment of sunscreens. In line with its labeled 50+ SPF, the commercial test product confirmed its improved protection especially on DNA damage prevention.</p></div>","PeriodicalId":375,"journal":{"name":"Journal of Photochemistry and Photobiology","volume":"19 ","pages":"Article 100213"},"PeriodicalIF":3.2610,"publicationDate":"2023-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666469023000544/pdfft?md5=e9553983022c06745e3365bffb3b0059&pid=1-s2.0-S2666469023000544-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Use of reconstructed skin model to assess the photoprotection afforded by three sunscreen products having different SPF values against DNA lesions and cellular alterations\",\"authors\":\"D. Lelièvre , F. Canivet , F. Thillou , C. Tricaud , C. Le Floc'h , F. Bernerd\",\"doi\":\"10.1016/j.jpap.2023.100213\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Introduction</h3><p>Both UVB and UVA rays induce biological damages in the epidermis and the dermis that contribute to photo-carcinogenesis and photoaging. In the present study, the photoprotective effect of 2 ISO standard sunscreens, P3 (Sun Protection Factor [SPF]15) and P6 (SPF40) and of an SPF50+ labeled commercial sunscreen product was tested in reconstructed skin tissues exposed to increasing doses of UV Solar Simulated Radiation (UV-SSR). UV-induced damages were evaluated using several biological markers, including DNA lesions in the presence or absence of sunscreen protection.</p></div><div><h3>Method</h3><p>T-Skin™ model samples (EPISKIN), composed of a fibroblast-populated dermal equivalent and a fully differentiated epidermis, were protected with the test sunscreens (1.3 mg/cm² topically applied on molded polymethyl methacrylate plate) before being exposed to increasing UV doses (0 – 2.5 – 5 - 25 – 40 J/cm²). Twenty-four hours after exposure, tissues with and without sunscreen protection, were analyzed for skin viability and morphology, DNA lesions (cyclobutane pyrimidine dimer) and inflammatory mediator quantification. Results were compared to untreated exposed tissues using a Wilcoxon non-parametric test.</p></div><div><h3>Results</h3><p>For untreated tissues, UV-SSR exposure induced a dose-dependent decrease in epidermal and dermal viabilities, an increase in release of proinflammatory cytokines and matrix metalloproteinases and were associated with morphological damages at doses as low as 5 J/cm<sup>2</sup>. DNA lesions were even detected at the lowest dose of 2.5 J/cm<sup>2</sup>, and their number increased with the UV-SSR dose. In the samples protected with sunscreens, these abnormalities were partially or totally prevented with P6 providing a better protection compared to P3, and the SPF50+ sunscreen showing a trend for better protection than P6, for example against DNA damage.</p></div><div><h3>Conclusions</h3><p>This study demonstrates that photoprotective effects of different sunscreens can be discriminated and ranked on reconstructed skin tissues (T-Skin™ model) exposed to UV-SSR. Showing significant differences between the reference products P3 and P6 in line with their respective SPF values, such study allows the evaluation of epidermal and dermal damages at the tissue, cellular and molecular levels. It thus opens the way to a new model of integrated assessment of sunscreens. In line with its labeled 50+ SPF, the commercial test product confirmed its improved protection especially on DNA damage prevention.</p></div>\",\"PeriodicalId\":375,\"journal\":{\"name\":\"Journal of Photochemistry and Photobiology\",\"volume\":\"19 \",\"pages\":\"Article 100213\"},\"PeriodicalIF\":3.2610,\"publicationDate\":\"2023-11-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S2666469023000544/pdfft?md5=e9553983022c06745e3365bffb3b0059&pid=1-s2.0-S2666469023000544-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Photochemistry and Photobiology\",\"FirstCategoryId\":\"2\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2666469023000544\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Photochemistry and Photobiology","FirstCategoryId":"2","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2666469023000544","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Use of reconstructed skin model to assess the photoprotection afforded by three sunscreen products having different SPF values against DNA lesions and cellular alterations
Introduction
Both UVB and UVA rays induce biological damages in the epidermis and the dermis that contribute to photo-carcinogenesis and photoaging. In the present study, the photoprotective effect of 2 ISO standard sunscreens, P3 (Sun Protection Factor [SPF]15) and P6 (SPF40) and of an SPF50+ labeled commercial sunscreen product was tested in reconstructed skin tissues exposed to increasing doses of UV Solar Simulated Radiation (UV-SSR). UV-induced damages were evaluated using several biological markers, including DNA lesions in the presence or absence of sunscreen protection.
Method
T-Skin™ model samples (EPISKIN), composed of a fibroblast-populated dermal equivalent and a fully differentiated epidermis, were protected with the test sunscreens (1.3 mg/cm² topically applied on molded polymethyl methacrylate plate) before being exposed to increasing UV doses (0 – 2.5 – 5 - 25 – 40 J/cm²). Twenty-four hours after exposure, tissues with and without sunscreen protection, were analyzed for skin viability and morphology, DNA lesions (cyclobutane pyrimidine dimer) and inflammatory mediator quantification. Results were compared to untreated exposed tissues using a Wilcoxon non-parametric test.
Results
For untreated tissues, UV-SSR exposure induced a dose-dependent decrease in epidermal and dermal viabilities, an increase in release of proinflammatory cytokines and matrix metalloproteinases and were associated with morphological damages at doses as low as 5 J/cm2. DNA lesions were even detected at the lowest dose of 2.5 J/cm2, and their number increased with the UV-SSR dose. In the samples protected with sunscreens, these abnormalities were partially or totally prevented with P6 providing a better protection compared to P3, and the SPF50+ sunscreen showing a trend for better protection than P6, for example against DNA damage.
Conclusions
This study demonstrates that photoprotective effects of different sunscreens can be discriminated and ranked on reconstructed skin tissues (T-Skin™ model) exposed to UV-SSR. Showing significant differences between the reference products P3 and P6 in line with their respective SPF values, such study allows the evaluation of epidermal and dermal damages at the tissue, cellular and molecular levels. It thus opens the way to a new model of integrated assessment of sunscreens. In line with its labeled 50+ SPF, the commercial test product confirmed its improved protection especially on DNA damage prevention.