Carbon Monoxide Partially Mediates Protective Effect of Resveratrol Against UVB-Induced Oxidative Stress in Human Keratinocytes

Based on the antioxidative effect of resveratrol (RES) in mitigating reactive oxygen species (ROS) production through the induction of nuclear factor-erythroid 2-related factor-2 (Nrf2)/heme oxigenase-1 (HO-1) signaling pathway, we investigated whether the protective activity of RES against ROS-medi...

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Main Authors: Janice N. Averilla, Jisun Oh, Jong-Sang Kim
Format: Article
Language:English
Published: MDPI AG 2019-10-01
Series:Antioxidants
Subjects:
Online Access:https://www.mdpi.com/2076-3921/8/10/432
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author Janice N. Averilla
Jisun Oh
Jong-Sang Kim
author_facet Janice N. Averilla
Jisun Oh
Jong-Sang Kim
author_sort Janice N. Averilla
collection DOAJ
description Based on the antioxidative effect of resveratrol (RES) in mitigating reactive oxygen species (ROS) production through the induction of nuclear factor-erythroid 2-related factor-2 (Nrf2)/heme oxigenase-1 (HO-1) signaling pathway, we investigated whether the protective activity of RES against ROS-mediated cytotoxicity is mediated by intracellular carbon monoxide (CO), a product of HO-1 activity, in ultraviolet B (UVB)-irradiated human keratinocyte HaCaT cells. The cells were exposed to UVB radiation following treatment with RES and/or CO-releasing molecule-2 (CORM-2). RES and/or CORM-2 upregulated HO-1 protein expression, accompanied by a gradual reduction of UVB-induced intracellular ROS levels. CORM-2 reduced intracellular ROS in the presence of tin protoporphyrin IX, an HO-1 inhibitor, indicating that the cytoprotection observed was mediated by intracellular CO and not by HO-1 itself. Moreover, CORM-2 decreased RES-stimulated mitochondrial quantity and respiration and increased the cytosolic protein expressions of radical-scavenging superoxide dismutases, SOD1 and SOD2. Taken together, our observations suggest that RES and intracellular CO act independently, at least partly, in attenuating cellular oxidative stress by promoting antioxidant enzyme expressions and inhibiting mitochondrial respiration in UVB-exposed keratinocytes.
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spelling doaj.art-a66b856408f7429d9a5e9db8c26dede82023-09-02T22:24:30ZengMDPI AGAntioxidants2076-39212019-10-0181043210.3390/antiox8100432antiox8100432Carbon Monoxide Partially Mediates Protective Effect of Resveratrol Against UVB-Induced Oxidative Stress in Human KeratinocytesJanice N. Averilla0Jisun Oh1Jong-Sang Kim2School of Food Science and Biotechnology (BK21 Plus), Kyungpook National University, Daegu 41566, KoreaInstitute of Agricultural Science and Technology, Kyungpook National University, Daegu 41566, KoreaSchool of Food Science and Biotechnology (BK21 Plus), Kyungpook National University, Daegu 41566, KoreaBased on the antioxidative effect of resveratrol (RES) in mitigating reactive oxygen species (ROS) production through the induction of nuclear factor-erythroid 2-related factor-2 (Nrf2)/heme oxigenase-1 (HO-1) signaling pathway, we investigated whether the protective activity of RES against ROS-mediated cytotoxicity is mediated by intracellular carbon monoxide (CO), a product of HO-1 activity, in ultraviolet B (UVB)-irradiated human keratinocyte HaCaT cells. The cells were exposed to UVB radiation following treatment with RES and/or CO-releasing molecule-2 (CORM-2). RES and/or CORM-2 upregulated HO-1 protein expression, accompanied by a gradual reduction of UVB-induced intracellular ROS levels. CORM-2 reduced intracellular ROS in the presence of tin protoporphyrin IX, an HO-1 inhibitor, indicating that the cytoprotection observed was mediated by intracellular CO and not by HO-1 itself. Moreover, CORM-2 decreased RES-stimulated mitochondrial quantity and respiration and increased the cytosolic protein expressions of radical-scavenging superoxide dismutases, SOD1 and SOD2. Taken together, our observations suggest that RES and intracellular CO act independently, at least partly, in attenuating cellular oxidative stress by promoting antioxidant enzyme expressions and inhibiting mitochondrial respiration in UVB-exposed keratinocytes.https://www.mdpi.com/2076-3921/8/10/432resveratrolheme oxygenasecarbon monoxidemitochondriauvb irradiationkeratinocytes
spellingShingle Janice N. Averilla
Jisun Oh
Jong-Sang Kim
Carbon Monoxide Partially Mediates Protective Effect of Resveratrol Against UVB-Induced Oxidative Stress in Human Keratinocytes
Antioxidants
resveratrol
heme oxygenase
carbon monoxide
mitochondria
uvb irradiation
keratinocytes
title Carbon Monoxide Partially Mediates Protective Effect of Resveratrol Against UVB-Induced Oxidative Stress in Human Keratinocytes
title_full Carbon Monoxide Partially Mediates Protective Effect of Resveratrol Against UVB-Induced Oxidative Stress in Human Keratinocytes
title_fullStr Carbon Monoxide Partially Mediates Protective Effect of Resveratrol Against UVB-Induced Oxidative Stress in Human Keratinocytes
title_full_unstemmed Carbon Monoxide Partially Mediates Protective Effect of Resveratrol Against UVB-Induced Oxidative Stress in Human Keratinocytes
title_short Carbon Monoxide Partially Mediates Protective Effect of Resveratrol Against UVB-Induced Oxidative Stress in Human Keratinocytes
title_sort carbon monoxide partially mediates protective effect of resveratrol against uvb induced oxidative stress in human keratinocytes
topic resveratrol
heme oxygenase
carbon monoxide
mitochondria
uvb irradiation
keratinocytes
url https://www.mdpi.com/2076-3921/8/10/432
work_keys_str_mv AT janicenaverilla carbonmonoxidepartiallymediatesprotectiveeffectofresveratrolagainstuvbinducedoxidativestressinhumankeratinocytes
AT jisunoh carbonmonoxidepartiallymediatesprotectiveeffectofresveratrolagainstuvbinducedoxidativestressinhumankeratinocytes
AT jongsangkim carbonmonoxidepartiallymediatesprotectiveeffectofresveratrolagainstuvbinducedoxidativestressinhumankeratinocytes