{"title":"1,25-二羟维生素D3可减轻紫外线b对人永生化角质形成细胞的损伤。","authors":"Pingwei Wang, Dongge Liu, Jiajing Cui, Shuqi Yan, Yujun Liang, Qianqian Chen, Yanping Liu, Shuping Ren, Peng Chen","doi":"10.1080/15569527.2023.2208676","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Ultraviolet-B (UVB) radiation is an important factor in causing skin damage. The study is to explore whether 1,25-Dihydroxvitamin D3(1,25(OH)<sub>2</sub>D<sub>3</sub>) will attenuate the damage of human immortalised keratinocytes (HaCaT) cells caused by UVB and relevant underlying mechanisms.</p><p><strong>Methods: </strong>CCK-8 was employed to determine the UVB irradiation intensity and 1,25(OH)<sub>2</sub>D<sub>3</sub> concentration. Western blot was used to detect the expression of NF-κB, Caspase9, Caspase3, Bax, Bcl2, FADD, CytC, Beclin-1; Flowcytometry was applied to measure the production of ROS.</p><p><strong>Results: </strong>The concentration of 1,25(OH)<sub>2</sub>D<sub>3</sub> used in the study was 100 nM and the UVB irradiation intensity was 20 mJ/cm<sup>2</sup>. Compared with the HaCaT cells irradiated with UVB, the HaCaT cells that were pre-treated with 1,25(OH)<sub>2</sub>D<sub>3</sub> had lower production of ROS, lower expression of NF-κB, Caspase9, Caspase3, Bax, FADD, CytC and Beclin-1(<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>1,25(OH)<sub>2</sub>D<sub>3</sub> could inhibit the development of oxidative stress and apoptosis in HaCaTs triggered by UVB. This inhibition might be achieved through the suppression of mitochondria-modulated apoptosis and autophagy. Vitamin D may be a potential UVB protective component.</p>","PeriodicalId":11023,"journal":{"name":"Cutaneous and Ocular Toxicology","volume":"42 2","pages":"74-81"},"PeriodicalIF":1.6000,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"1,25-Dihydroxvitamin D3 attenuates the damage of human immortalised keratinocytes caused by Ultraviolet-B.\",\"authors\":\"Pingwei Wang, Dongge Liu, Jiajing Cui, Shuqi Yan, Yujun Liang, Qianqian Chen, Yanping Liu, Shuping Ren, Peng Chen\",\"doi\":\"10.1080/15569527.2023.2208676\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>Ultraviolet-B (UVB) radiation is an important factor in causing skin damage. The study is to explore whether 1,25-Dihydroxvitamin D3(1,25(OH)<sub>2</sub>D<sub>3</sub>) will attenuate the damage of human immortalised keratinocytes (HaCaT) cells caused by UVB and relevant underlying mechanisms.</p><p><strong>Methods: </strong>CCK-8 was employed to determine the UVB irradiation intensity and 1,25(OH)<sub>2</sub>D<sub>3</sub> concentration. Western blot was used to detect the expression of NF-κB, Caspase9, Caspase3, Bax, Bcl2, FADD, CytC, Beclin-1; Flowcytometry was applied to measure the production of ROS.</p><p><strong>Results: </strong>The concentration of 1,25(OH)<sub>2</sub>D<sub>3</sub> used in the study was 100 nM and the UVB irradiation intensity was 20 mJ/cm<sup>2</sup>. Compared with the HaCaT cells irradiated with UVB, the HaCaT cells that were pre-treated with 1,25(OH)<sub>2</sub>D<sub>3</sub> had lower production of ROS, lower expression of NF-κB, Caspase9, Caspase3, Bax, FADD, CytC and Beclin-1(<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>1,25(OH)<sub>2</sub>D<sub>3</sub> could inhibit the development of oxidative stress and apoptosis in HaCaTs triggered by UVB. This inhibition might be achieved through the suppression of mitochondria-modulated apoptosis and autophagy. Vitamin D may be a potential UVB protective component.</p>\",\"PeriodicalId\":11023,\"journal\":{\"name\":\"Cutaneous and Ocular Toxicology\",\"volume\":\"42 2\",\"pages\":\"74-81\"},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2023-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cutaneous and Ocular Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/15569527.2023.2208676\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"OPHTHALMOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cutaneous and Ocular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/15569527.2023.2208676","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"OPHTHALMOLOGY","Score":null,"Total":0}
1,25-Dihydroxvitamin D3 attenuates the damage of human immortalised keratinocytes caused by Ultraviolet-B.
Objective: Ultraviolet-B (UVB) radiation is an important factor in causing skin damage. The study is to explore whether 1,25-Dihydroxvitamin D3(1,25(OH)2D3) will attenuate the damage of human immortalised keratinocytes (HaCaT) cells caused by UVB and relevant underlying mechanisms.
Methods: CCK-8 was employed to determine the UVB irradiation intensity and 1,25(OH)2D3 concentration. Western blot was used to detect the expression of NF-κB, Caspase9, Caspase3, Bax, Bcl2, FADD, CytC, Beclin-1; Flowcytometry was applied to measure the production of ROS.
Results: The concentration of 1,25(OH)2D3 used in the study was 100 nM and the UVB irradiation intensity was 20 mJ/cm2. Compared with the HaCaT cells irradiated with UVB, the HaCaT cells that were pre-treated with 1,25(OH)2D3 had lower production of ROS, lower expression of NF-κB, Caspase9, Caspase3, Bax, FADD, CytC and Beclin-1(P < 0.05).
Conclusion: 1,25(OH)2D3 could inhibit the development of oxidative stress and apoptosis in HaCaTs triggered by UVB. This inhibition might be achieved through the suppression of mitochondria-modulated apoptosis and autophagy. Vitamin D may be a potential UVB protective component.
期刊介绍：
Cutaneous and Ocular Toxicology is an international, peer-reviewed journal that covers all types of harm to cutaneous and ocular systems. Areas of particular interest include pharmaceutical and medical products; consumer, personal care, and household products; and issues in environmental and occupational exposures.
In addition to original research papers, reviews and short communications are invited, as well as concise, relevant, and critical reviews of topics of contemporary significance.
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