Yuna Kim, Junbo Sim, Kyungeun Jeon, Dehun Ryu, Youngeun Ji, Youngseok Kim, Junoh Kim, Suwon Jeon, Deokhoon Park, Eunsun Jung
{"title":"发酵黑参提取物通过调节人角质形成细胞的nc886-PKR通路来预防uvb诱导的炎症。","authors":"Yuna Kim, Junbo Sim, Kyungeun Jeon, Dehun Ryu, Youngeun Ji, Youngseok Kim, Junoh Kim, Suwon Jeon, Deokhoon Park, Eunsun Jung","doi":"10.1111/phpp.12927","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Continuous exposure of the skin to ultraviolet B (UVB) rays can cause inflammation and photodamage. In previous studies, we observed that the upregulation of nc886, a noncoding RNA (ncRNA), can alleviate UVB-induced inflammation through suppression of the protein kinase RNA (PKR) pathway. We aim to investigate the effect of fermented black ginseng extract (FBGE), which has been shown to increase the expression of nc886, on UVB-induced inflammation in keratinocytes.</p><p><strong>Methods: </strong>To confirm the cytotoxicity of FBGE, MTT assay was performed, and no significant cytotoxicity was found on human keratinocytes. The efficacies of FBGE were assessed through qPCR, Western blotting, and ELISA analysis which confirmed regulation of UVB-induced inflammation.</p><p><strong>Results: </strong>The analysis results showed that FBGE inhibited the decrease in nc886 expression and the increase in the methylated nc886 caused by UVB. It also prevented the UVB-induced increase of metalloproteinase-9 (MMP-9), metalloproteinase-1 (MMP-1), cyclooxygenase-2 (COX-2), prostaglandin E<sub>2</sub> (PGE2), interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α). Additionally, FBGE suppressed the PKR-MAPK pathways activated by UVB.</p><p><strong>Conclusion: </strong>These results implicate that FBGE can alleviate UVB-induced inflammation through regulation of the nc886-PKR pathway.</p>","PeriodicalId":20123,"journal":{"name":"Photodermatology, photoimmunology & photomedicine","volume":null,"pages":null},"PeriodicalIF":2.5000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Fermented black ginseng extract prevents UVB-induced inflammation by regulating the nc886-PKR pathway in human keratinocytes.\",\"authors\":\"Yuna Kim, Junbo Sim, Kyungeun Jeon, Dehun Ryu, Youngeun Ji, Youngseok Kim, Junoh Kim, Suwon Jeon, Deokhoon Park, Eunsun Jung\",\"doi\":\"10.1111/phpp.12927\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Continuous exposure of the skin to ultraviolet B (UVB) rays can cause inflammation and photodamage. In previous studies, we observed that the upregulation of nc886, a noncoding RNA (ncRNA), can alleviate UVB-induced inflammation through suppression of the protein kinase RNA (PKR) pathway. We aim to investigate the effect of fermented black ginseng extract (FBGE), which has been shown to increase the expression of nc886, on UVB-induced inflammation in keratinocytes.</p><p><strong>Methods: </strong>To confirm the cytotoxicity of FBGE, MTT assay was performed, and no significant cytotoxicity was found on human keratinocytes. The efficacies of FBGE were assessed through qPCR, Western blotting, and ELISA analysis which confirmed regulation of UVB-induced inflammation.</p><p><strong>Results: </strong>The analysis results showed that FBGE inhibited the decrease in nc886 expression and the increase in the methylated nc886 caused by UVB. It also prevented the UVB-induced increase of metalloproteinase-9 (MMP-9), metalloproteinase-1 (MMP-1), cyclooxygenase-2 (COX-2), prostaglandin E<sub>2</sub> (PGE2), interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α). Additionally, FBGE suppressed the PKR-MAPK pathways activated by UVB.</p><p><strong>Conclusion: </strong>These results implicate that FBGE can alleviate UVB-induced inflammation through regulation of the nc886-PKR pathway.</p>\",\"PeriodicalId\":20123,\"journal\":{\"name\":\"Photodermatology, photoimmunology & photomedicine\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Photodermatology, photoimmunology & photomedicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1111/phpp.12927\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/11/14 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"DERMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Photodermatology, photoimmunology & photomedicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/phpp.12927","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/11/14 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"DERMATOLOGY","Score":null,"Total":0}
Fermented black ginseng extract prevents UVB-induced inflammation by regulating the nc886-PKR pathway in human keratinocytes.
Background: Continuous exposure of the skin to ultraviolet B (UVB) rays can cause inflammation and photodamage. In previous studies, we observed that the upregulation of nc886, a noncoding RNA (ncRNA), can alleviate UVB-induced inflammation through suppression of the protein kinase RNA (PKR) pathway. We aim to investigate the effect of fermented black ginseng extract (FBGE), which has been shown to increase the expression of nc886, on UVB-induced inflammation in keratinocytes.
Methods: To confirm the cytotoxicity of FBGE, MTT assay was performed, and no significant cytotoxicity was found on human keratinocytes. The efficacies of FBGE were assessed through qPCR, Western blotting, and ELISA analysis which confirmed regulation of UVB-induced inflammation.
Results: The analysis results showed that FBGE inhibited the decrease in nc886 expression and the increase in the methylated nc886 caused by UVB. It also prevented the UVB-induced increase of metalloproteinase-9 (MMP-9), metalloproteinase-1 (MMP-1), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α). Additionally, FBGE suppressed the PKR-MAPK pathways activated by UVB.
Conclusion: These results implicate that FBGE can alleviate UVB-induced inflammation through regulation of the nc886-PKR pathway.
期刊介绍:
The journal is a forum for new information about the direct and distant effects of electromagnetic radiation (ultraviolet, visible and infrared) mediated through skin. The divisions of the editorial board reflect areas of specific interest: aging, carcinogenesis, immunology, instrumentation and optics, lasers, photodynamic therapy, photosensitivity, pigmentation and therapy. Photodermatology, Photoimmunology & Photomedicine includes original articles, reviews, communications and editorials.
Original articles may include the investigation of experimental or pathological processes in humans or animals in vivo or the investigation of radiation effects in cells or tissues in vitro. Methodology need have no limitation; rather, it should be appropriate to the question addressed.