{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T21:45:06Z","timestamp":1790631906704,"version":"4.1.0"},"reference-count":35,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,3,11]],"date-time":"2022-03-11T00:00:00Z","timestamp":1646956800000},"content-version":"vor","delay-in-days":69,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81402587"],"award-info":[{"award-number":["81402587"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81773310"],"award-info":[{"award-number":["81773310"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:p>\n                    Vitiligo is an acquired skin depigmentation disease in which excessive reactive oxygen species (ROS) play a critical pathogenic role in melanocyte destruction. The complex crosstalk between melanocytes and keratinocytes in vitiligo suggests that treatments aimed at protecting both the cells might be meaningful. In this study, we investigated the effect of 4\u2010octyl itaconate (4\u2010OI), an itaconate derivative, on ultraviolet B\u2010 (UVB\u2010) induced apoptosis in HaCaT and PIG1 cells and the underlying mechanisms. HaCaT and PIG1 cells were pretreated with 4\u2010OI (50 or 100\u2009\n                    <jats:italic>\u03bc<\/jats:italic>\n                    M) for 24\u2009h and then exposed to 300\u2009mJ\/cm\n                    <jats:sup>2<\/jats:sup>\n                    UVB (emission range 290\u2013320\u2009nm, emission peak 310\u2009nm). ROS levels and cell apoptosis were investigated using fluorescence microscopy and flow cytometry 24\u2009h after irradiation. In addition, nuclear translocation and the expression of pathway\u2010related proteins and mRNAs were detected using confocal microscopy, western blotting, and qRT\u2010PCR, respectively. Our results demonstrated that UVB induced apoptosis in HaCaT and PIG1 cells, whereas inhibition of ROS production could reverse this effect. Furthermore, 4\u2010OI attenuated UVB\u2010induced apoptosis in HaCaT and PIG1 cells in a concentration\u2010dependent manner by reducing the ROS levels. Moreover, 4\u2010OI induced nuclear translocation and activation of nuclear factor erythroid 2\u2010related factor 2 (Nrf2), and Nrf2 silencing reversed the inhibitory effect of 4\u2010OI on the UVB\u2010induced increase in ROS production and apoptosis in HaCaT and PIG1 cells. In addition,\n                    <jats:italic>in vivo<\/jats:italic>\n                    experiments using the Institute of Cancer Research mouse model showed that 4\u2010OI\n                    <jats:italic>via<\/jats:italic>\n                    tail vein injection (10\u2009mg\/kg\/day for six consecutive days) could reduce skin damage induced by UVB (400\u2009mJ\/cm\n                    <jats:sup>2<\/jats:sup>\n                    \/day for five consecutive days). In conclusion, 4\u2010OI can protect melanocytes and keratinocytes from UVB\u2010induced apoptosis by Nrf2 activation\u2010dependent ROS inhibition and can potentially treat skin disorders associated with oxidative stress, such as vitiligo.\n                  <\/jats:p>","DOI":"10.1155\/2022\/9897442","type":"journal-article","created":{"date-parts":[[2022,3,11]],"date-time":"2022-03-11T18:35:25Z","timestamp":1647023725000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Four\u2010Octyl Itaconate Attenuates UVB\u2010Induced Melanocytes and Keratinocytes Apoptosis by Nrf2 Activation\u2010Dependent ROS 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