MitoPlantRedoxV1, Main, Exploration, bibRecord, 000236

Baicalein protects human vitiligo melanocytes from oxidative stress through activation of NF-E2-related factor2 (Nrf2) signaling pathway.

Identifieur interne : 000236 ( Main/Exploration ); précédent : 000235; suivant : 000237

Baicalein protects human vitiligo melanocytes from oxidative stress through activation of NF-E2-related factor2 (Nrf2) signaling pathway.

Source :

Free radical biology & medicine [ 1873-4596 ] ; 2018.

RBID : pubmed:30342186

Descripteurs français

KwdFr :
- Antioxydants (isolement et purification), Antioxydants (pharmacologie), Extraits de plantes (composition chimique), Facteur-2 apparenté à NF-E2 (antagonistes et inhibiteurs), Facteur-2 apparenté à NF-E2 (génétique), Facteur-2 apparenté à NF-E2 (métabolisme), Flavanones (isolement et purification), Flavanones (pharmacologie), Heme oxygenase-1 (génétique), Heme oxygenase-1 (métabolisme), Humains (MeSH), Lignée cellulaire (MeSH), Mitochondries (effets des médicaments et des substances chimiques), Mitochondries (métabolisme), Mitogen-Activated Protein Kinase 1 (génétique), Mitogen-Activated Protein Kinase 1 (métabolisme), Mitogen-Activated Protein Kinase 3 (génétique), Mitogen-Activated Protein Kinase 3 (métabolisme), Mélanocytes (anatomopathologie), Mélanocytes (effets des médicaments et des substances chimiques), Mélanocytes (métabolisme), Peroxyde d'hydrogène (antagonistes et inhibiteurs), Peroxyde d'hydrogène (pharmacologie), Petit ARN interférent (génétique), Petit ARN interférent (métabolisme), Phosphatidylinositol 3-kinases (génétique), Phosphatidylinositol 3-kinases (métabolisme), Protéines proto-oncogènes c-akt (génétique), Protéines proto-oncogènes c-akt (métabolisme), Régulation de l'expression des gènes (MeSH), Scutellaria baicalensis (composition chimique), Stress oxydatif (MeSH), Transduction du signal (effets des médicaments et des substances chimiques), Transduction du signal (génétique), Vitiligo (anatomopathologie), Vitiligo (génétique), Vitiligo (métabolisme).
MESH :
- anatomopathologie : Mélanocytes, Vitiligo.
- antagonistes et inhibiteurs : Facteur-2 apparenté à NF-E2, Peroxyde d'hydrogène.
- composition chimique : Extraits de plantes, Scutellaria baicalensis.
- effets des médicaments et des substances chimiques : Mitochondries, Mélanocytes, Transduction du signal.
- génétique : Facteur-2 apparenté à NF-E2, Heme oxygenase-1, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Petit ARN interférent, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt, Transduction du signal, Vitiligo.
- isolement et purification : Antioxydants, Flavanones.
- métabolisme : Facteur-2 apparenté à NF-E2, Heme oxygenase-1, Mitochondries, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Mélanocytes, Petit ARN interférent, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt, Vitiligo.
- pharmacologie : Antioxydants, Flavanones, Peroxyde d'hydrogène.
- Humains, Lignée cellulaire, Régulation de l'expression des gènes, Stress oxydatif.

English descriptors

KwdEn :
- Antioxidants (isolation & purification), Antioxidants (pharmacology), Cell Line (MeSH), Flavanones (isolation & purification), Flavanones (pharmacology), Gene Expression Regulation (MeSH), Heme Oxygenase-1 (genetics), Heme Oxygenase-1 (metabolism), Humans (MeSH), Hydrogen Peroxide (antagonists & inhibitors), Hydrogen Peroxide (pharmacology), Melanocytes (drug effects), Melanocytes (metabolism), Melanocytes (pathology), Mitochondria (drug effects), Mitochondria (metabolism), Mitogen-Activated Protein Kinase 1 (genetics), Mitogen-Activated Protein Kinase 1 (metabolism), Mitogen-Activated Protein Kinase 3 (genetics), Mitogen-Activated Protein Kinase 3 (metabolism), NF-E2-Related Factor 2 (antagonists & inhibitors), NF-E2-Related Factor 2 (genetics), NF-E2-Related Factor 2 (metabolism), Oxidative Stress (MeSH), Phosphatidylinositol 3-Kinases (genetics), Phosphatidylinositol 3-Kinases (metabolism), Plant Extracts (chemistry), Proto-Oncogene Proteins c-akt (genetics), Proto-Oncogene Proteins c-akt (metabolism), RNA, Small Interfering (genetics), RNA, Small Interfering (metabolism), Scutellaria baicalensis (chemistry), Signal Transduction (drug effects), Signal Transduction (genetics), Vitiligo (genetics), Vitiligo (metabolism), Vitiligo (pathology).
MESH :
- chemical , antagonists & inhibitors : Hydrogen Peroxide, NF-E2-Related Factor 2.
- chemical , chemistry : Plant Extracts.
- chemical , genetics : Heme Oxygenase-1, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, NF-E2-Related Factor 2, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, RNA, Small Interfering.
- chemical , isolation & purification : Antioxidants, Flavanones.
- chemical , metabolism : Heme Oxygenase-1, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, NF-E2-Related Factor 2, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, RNA, Small Interfering.
- chemical , pharmacology : Antioxidants, Flavanones, Hydrogen Peroxide.
- chemistry : Scutellaria baicalensis.
- drug effects : Melanocytes, Mitochondria, Signal Transduction.
- genetics : Signal Transduction, Vitiligo.
- metabolism : Melanocytes, Mitochondria, Vitiligo.
- pathology : Melanocytes, Vitiligo.
- Cell Line, Gene Expression Regulation, Humans, Oxidative Stress.

Abstract

Vitiligo is a complex disorder characterized by patchy loss of skin pigmentation due to abnormal melanocyte function. Overwhelming evidences have suggested that oxidative stress plays a major role in the loss of melanocytes thereby mediating the onset and progression of vitiligo. The nuclear factor erythroid 2-like factor 2 (Nrf2) is a master regulator of cellular redox homeostasis and the activation of Nrf2 signaling pathway is impaired in the vitiligo melanocytes. Baicalein, as flavonoid extracted from the Scutellaria baicalensis, has been proved to possess the ability to activate Nrf2 signaling pathway in other cell types and mouse model. Our previous data found that baicalein exerts a cytoprotective role in H₂O₂-induced apoptosis in human melanocytes cell line (PIG1). Based on these founding, we hypothesized that baicalein activates Nrf2 signaling pathway, alleviates H₂O₂-induced mitochondrial dysfunction and cellular damage, thereby protecting human vitiligo melanocytes from oxidative stress. In the present study, we found that baicalein effectively inhibited H₂O₂-induced cytotoxicity and apoptosis in human vitiligo melanocytes (PIG3V). Further results demonstrated that baicalein promoted Nrf2 nucleus translocation as well as up-regulated the expression of Nrf2 and its target gene, heme oxygenase-1 (HO-1). Moreover, the protective effects of baicalein against H₂O₂-induced cellular damage and apoptosis as well as mitochondrial dysfunction were abolished by Nrf2 knockdown. Additionally, we observed that Nrf2 knockdown suppressed proliferation and increased the sensitivity of PIG3V cells to H₂O₂ treatment. Finally, we explored the mechanism of baicalein associated with Nrf2 activation and found that the phosphorylation of Nrf2 as well as ERK1/2and PI3K/AKT signaling were not involved in the baicalein-induced activation of Nrf2. Taken together, these data clearly suggest that baicalein enhances cellular antioxidant defense capacity of human vitiligo melanocytes through the activation of the Nrf2 signaling pathway, providing beneficial evidence for the application of baicalein in the vitiligo treatment.

DOI: 10.1016/j.freeradbiomed.2018.10.421
PubMed: 30342186

Affiliations:

République populaire de Chine

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to stream Main, to step Corpus: 000168
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Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en">Baicalein protects human vitiligo melanocytes from oxidative stress through activation of NF-E2-related factor2 (Nrf2) signaling pathway.</title>
<author><name sortKey="Ma, Jingjing" sort="Ma, Jingjing" uniqKey="Ma J" first="Jingjing" last="Ma">Jingjing Ma</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Li, Shuli" sort="Li, Shuli" uniqKey="Li S" first="Shuli" last="Li">Shuli Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
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<author><name sortKey="Zhu, Longfei" sort="Zhu, Longfei" uniqKey="Zhu L" first="Longfei" last="Zhu">Longfei Zhu</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
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<author><name sortKey="Guo, Sen" sort="Guo, Sen" uniqKey="Guo S" first="Sen" last="Guo">Sen Guo</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
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<author><name sortKey="Yi, Xiuli" sort="Yi, Xiuli" uniqKey="Yi X" first="Xiuli" last="Yi">Xiuli Yi</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
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<author><name sortKey="Cui, Tingting" sort="Cui, Tingting" uniqKey="Cui T" first="Tingting" last="Cui">Tingting Cui</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
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<author><name sortKey="He, Yuanmin" sort="He, Yuanmin" uniqKey="He Y" first="Yuanmin" last="He">Yuanmin He</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Chang, Yuqian" sort="Chang, Yuqian" uniqKey="Chang Y" first="Yuqian" last="Chang">Yuqian Chang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Liu, Bangmin" sort="Liu, Bangmin" uniqKey="Liu B" first="Bangmin" last="Liu">Bangmin Liu</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China. Electronic address: lbm009@163.com.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Li, Chunying" sort="Li, Chunying" uniqKey="Li C" first="Chunying" last="Li">Chunying Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China. Electronic address: lichying@fmmu.edu.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Jian, Zhe" sort="Jian, Zhe" uniqKey="Jian Z" first="Zhe" last="Jian">Zhe Jian</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China. Electronic address: xjzhejian@fmmu.edu.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
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<imprint><date when="2018" type="published">2018</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antioxidants (isolation & purification)</term>
<term>Antioxidants (pharmacology)</term>
<term>Cell Line (MeSH)</term>
<term>Flavanones (isolation & purification)</term>
<term>Flavanones (pharmacology)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Heme Oxygenase-1 (genetics)</term>
<term>Heme Oxygenase-1 (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Hydrogen Peroxide (antagonists & inhibitors)</term>
<term>Hydrogen Peroxide (pharmacology)</term>
<term>Melanocytes (drug effects)</term>
<term>Melanocytes (metabolism)</term>
<term>Melanocytes (pathology)</term>
<term>Mitochondria (drug effects)</term>
<term>Mitochondria (metabolism)</term>
<term>Mitogen-Activated Protein Kinase 1 (genetics)</term>
<term>Mitogen-Activated Protein Kinase 1 (metabolism)</term>
<term>Mitogen-Activated Protein Kinase 3 (genetics)</term>
<term>Mitogen-Activated Protein Kinase 3 (metabolism)</term>
<term>NF-E2-Related Factor 2 (antagonists & inhibitors)</term>
<term>NF-E2-Related Factor 2 (genetics)</term>
<term>NF-E2-Related Factor 2 (metabolism)</term>
<term>Oxidative Stress (MeSH)</term>
<term>Phosphatidylinositol 3-Kinases (genetics)</term>
<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Plant Extracts (chemistry)</term>
<term>Proto-Oncogene Proteins c-akt (genetics)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>RNA, Small Interfering (genetics)</term>
<term>RNA, Small Interfering (metabolism)</term>
<term>Scutellaria baicalensis (chemistry)</term>
<term>Signal Transduction (drug effects)</term>
<term>Signal Transduction (genetics)</term>
<term>Vitiligo (genetics)</term>
<term>Vitiligo (metabolism)</term>
<term>Vitiligo (pathology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Antioxydants (isolement et purification)</term>
<term>Antioxydants (pharmacologie)</term>
<term>Extraits de plantes (composition chimique)</term>
<term>Facteur-2 apparenté à NF-E2 (antagonistes et inhibiteurs)</term>
<term>Facteur-2 apparenté à NF-E2 (génétique)</term>
<term>Facteur-2 apparenté à NF-E2 (métabolisme)</term>
<term>Flavanones (isolement et purification)</term>
<term>Flavanones (pharmacologie)</term>
<term>Heme oxygenase-1 (génétique)</term>
<term>Heme oxygenase-1 (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Mitochondries (effets des médicaments et des substances chimiques)</term>
<term>Mitochondries (métabolisme)</term>
<term>Mitogen-Activated Protein Kinase 1 (génétique)</term>
<term>Mitogen-Activated Protein Kinase 1 (métabolisme)</term>
<term>Mitogen-Activated Protein Kinase 3 (génétique)</term>
<term>Mitogen-Activated Protein Kinase 3 (métabolisme)</term>
<term>Mélanocytes (anatomopathologie)</term>
<term>Mélanocytes (effets des médicaments et des substances chimiques)</term>
<term>Mélanocytes (métabolisme)</term>
<term>Peroxyde d'hydrogène (antagonistes et inhibiteurs)</term>
<term>Peroxyde d'hydrogène (pharmacologie)</term>
<term>Petit ARN interférent (génétique)</term>
<term>Petit ARN interférent (métabolisme)</term>
<term>Phosphatidylinositol 3-kinases (génétique)</term>
<term>Phosphatidylinositol 3-kinases (métabolisme)</term>
<term>Protéines proto-oncogènes c-akt (génétique)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Scutellaria baicalensis (composition chimique)</term>
<term>Stress oxydatif (MeSH)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>Transduction du signal (génétique)</term>
<term>Vitiligo (anatomopathologie)</term>
<term>Vitiligo (génétique)</term>
<term>Vitiligo (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Hydrogen Peroxide</term>
<term>NF-E2-Related Factor 2</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Plant Extracts</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Heme Oxygenase-1</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>NF-E2-Related Factor 2</term>
<term>Phosphatidylinositol 3-Kinases</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="isolation & purification" xml:lang="en"><term>Antioxidants</term>
<term>Flavanones</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Heme Oxygenase-1</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>NF-E2-Related Factor 2</term>
<term>Phosphatidylinositol 3-Kinases</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antioxidants</term>
<term>Flavanones</term>
<term>Hydrogen Peroxide</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Mélanocytes</term>
<term>Vitiligo</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteur-2 apparenté à NF-E2</term>
<term>Peroxyde d'hydrogène</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Scutellaria baicalensis</term>
</keywords>
<keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Extraits de plantes</term>
<term>Scutellaria baicalensis</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Melanocytes</term>
<term>Mitochondria</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Mitochondries</term>
<term>Mélanocytes</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Signal Transduction</term>
<term>Vitiligo</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur-2 apparenté à NF-E2</term>
<term>Heme oxygenase-1</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>Petit ARN interférent</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Transduction du signal</term>
<term>Vitiligo</term>
</keywords>
<keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr"><term>Antioxydants</term>
<term>Flavanones</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Melanocytes</term>
<term>Mitochondria</term>
<term>Vitiligo</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur-2 apparenté à NF-E2</term>
<term>Heme oxygenase-1</term>
<term>Mitochondries</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>Mélanocytes</term>
<term>Petit ARN interférent</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Vitiligo</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Melanocytes</term>
<term>Vitiligo</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antioxydants</term>
<term>Flavanones</term>
<term>Peroxyde d'hydrogène</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line</term>
<term>Gene Expression Regulation</term>
<term>Humans</term>
<term>Oxidative Stress</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
<term>Lignée cellulaire</term>
<term>Régulation de l'expression des gènes</term>
<term>Stress oxydatif</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Vitiligo is a complex disorder characterized by patchy loss of skin pigmentation due to abnormal melanocyte function. Overwhelming evidences have suggested that oxidative stress plays a major role in the loss of melanocytes thereby mediating the onset and progression of vitiligo. The nuclear factor erythroid 2-like factor 2 (Nrf2) is a master regulator of cellular redox homeostasis and the activation of Nrf2 signaling pathway is impaired in the vitiligo melanocytes. Baicalein, as flavonoid extracted from the Scutellaria baicalensis, has been proved to possess the ability to activate Nrf2 signaling pathway in other cell types and mouse model. Our previous data found that baicalein exerts a cytoprotective role in H<sub>2</sub>
O<sub>2</sub>
-induced apoptosis in human melanocytes cell line (PIG1). Based on these founding, we hypothesized that baicalein activates Nrf2 signaling pathway, alleviates H<sub>2</sub>
O<sub>2</sub>
-induced mitochondrial dysfunction and cellular damage, thereby protecting human vitiligo melanocytes from oxidative stress. In the present study, we found that baicalein effectively inhibited H<sub>2</sub>
O<sub>2</sub>
-induced cytotoxicity and apoptosis in human vitiligo melanocytes (PIG3V). Further results demonstrated that baicalein promoted Nrf2 nucleus translocation as well as up-regulated the expression of Nrf2 and its target gene, heme oxygenase-1 (HO-1). Moreover, the protective effects of baicalein against H<sub>2</sub>
O<sub>2</sub>
-induced cellular damage and apoptosis as well as mitochondrial dysfunction were abolished by Nrf2 knockdown. Additionally, we observed that Nrf2 knockdown suppressed proliferation and increased the sensitivity of PIG3V cells to H<sub>2</sub>
O<sub>2</sub>
 treatment. Finally, we explored the mechanism of baicalein associated with Nrf2 activation and found that the phosphorylation of Nrf2 as well as ERK1/2and PI3K/AKT signaling were not involved in the baicalein-induced activation of Nrf2. Taken together, these data clearly suggest that baicalein enhances cellular antioxidant defense capacity of human vitiligo melanocytes through the activation of the Nrf2 signaling pathway, providing beneficial evidence for the application of baicalein in the vitiligo treatment.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30342186</PMID>
<DateCompleted><Year>2019</Year>
<Month>09</Month>
<Day>27</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>09</Month>
<Day>27</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4596</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>129</Volume>
<PubDate><Year>2018</Year>
<Month>12</Month>
</PubDate>
</JournalIssue>
<Title>Free radical biology & medicine</Title>
<ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation>
</Journal>
<ArticleTitle>Baicalein protects human vitiligo melanocytes from oxidative stress through activation of NF-E2-related factor2 (Nrf2) signaling pathway.</ArticleTitle>
<Pagination><MedlinePgn>492-503</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S0891-5849(18)32194-4</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.freeradbiomed.2018.10.421</ELocationID>
<Abstract><AbstractText>Vitiligo is a complex disorder characterized by patchy loss of skin pigmentation due to abnormal melanocyte function. Overwhelming evidences have suggested that oxidative stress plays a major role in the loss of melanocytes thereby mediating the onset and progression of vitiligo. The nuclear factor erythroid 2-like factor 2 (Nrf2) is a master regulator of cellular redox homeostasis and the activation of Nrf2 signaling pathway is impaired in the vitiligo melanocytes. Baicalein, as flavonoid extracted from the Scutellaria baicalensis, has been proved to possess the ability to activate Nrf2 signaling pathway in other cell types and mouse model. Our previous data found that baicalein exerts a cytoprotective role in H<sub>2</sub>
O<sub>2</sub>
-induced apoptosis in human melanocytes cell line (PIG1). Based on these founding, we hypothesized that baicalein activates Nrf2 signaling pathway, alleviates H<sub>2</sub>
O<sub>2</sub>
-induced mitochondrial dysfunction and cellular damage, thereby protecting human vitiligo melanocytes from oxidative stress. In the present study, we found that baicalein effectively inhibited H<sub>2</sub>
O<sub>2</sub>
-induced cytotoxicity and apoptosis in human vitiligo melanocytes (PIG3V). Further results demonstrated that baicalein promoted Nrf2 nucleus translocation as well as up-regulated the expression of Nrf2 and its target gene, heme oxygenase-1 (HO-1). Moreover, the protective effects of baicalein against H<sub>2</sub>
O<sub>2</sub>
-induced cellular damage and apoptosis as well as mitochondrial dysfunction were abolished by Nrf2 knockdown. Additionally, we observed that Nrf2 knockdown suppressed proliferation and increased the sensitivity of PIG3V cells to H<sub>2</sub>
O<sub>2</sub>
 treatment. Finally, we explored the mechanism of baicalein associated with Nrf2 activation and found that the phosphorylation of Nrf2 as well as ERK1/2and PI3K/AKT signaling were not involved in the baicalein-induced activation of Nrf2. Taken together, these data clearly suggest that baicalein enhances cellular antioxidant defense capacity of human vitiligo melanocytes through the activation of the Nrf2 signaling pathway, providing beneficial evidence for the application of baicalein in the vitiligo treatment.</AbstractText>
<CopyrightInformation>Copyright © 2018 Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ma</LastName>
<ForeName>Jingjing</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Shuli</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhu</LastName>
<ForeName>Longfei</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Guo</LastName>
<ForeName>Sen</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yi</LastName>
<ForeName>Xiuli</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cui</LastName>
<ForeName>Tingting</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>He</LastName>
<ForeName>Yuanmin</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chang</LastName>
<ForeName>Yuqian</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Bangmin</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China. Electronic address: lbm009@163.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Chunying</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China. Electronic address: lichying@fmmu.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jian</LastName>
<ForeName>Zhe</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Dermatology, Xijing Hospital, Fourth Military Medical University, No. 127 Changlexi Road, Xi'an 710032, Shaanxi, China. Electronic address: xjzhejian@fmmu.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>10</Month>
<Day>18</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Free Radic Biol Med</MedlineTA>
<NlmUniqueID>8709159</NlmUniqueID>
<ISSNLinking>0891-5849</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D044950">Flavanones</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051267">NF-E2-Related Factor 2</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C495635">NFE2L2 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D010936">Plant Extracts</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>49QAH60606</RegistryNumber>
<NameOfSubstance UI="C006680">baicalein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>BBX060AN9V</RegistryNumber>
<NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.14.14.18</RegistryNumber>
<NameOfSubstance UI="C496541">HMOX1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.14.14.18</RegistryNumber>
<NameOfSubstance UI="D051547">Heme Oxygenase-1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber>
<NameOfSubstance UI="D019869">Phosphatidylinositol 3-Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber>
<NameOfSubstance UI="C535150">MAPK1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber>
<NameOfSubstance UI="C000629649">MAPK3 protein, human</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber>
<NameOfSubstance UI="D019950">Mitogen-Activated Protein Kinase 1</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber>
<NameOfSubstance UI="D048052">Mitogen-Activated Protein Kinase 3</NameOfSubstance>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000975" MajorTopicYN="N">Antioxidants</DescriptorName>
<QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D044950" MajorTopicYN="N">Flavanones</DescriptorName>
<QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051547" MajorTopicYN="N">Heme Oxygenase-1</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008544" MajorTopicYN="N">Melanocytes</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019950" MajorTopicYN="N">Mitogen-Activated Protein Kinase 1</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D048052" MajorTopicYN="N">Mitogen-Activated Protein Kinase 3</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051267" MajorTopicYN="N">NF-E2-Related Factor 2</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010936" MajorTopicYN="N">Plant Extracts</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D031364" MajorTopicYN="N">Scutellaria baicalensis</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014820" MajorTopicYN="N">Vitiligo</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Baicalein</Keyword>
<Keyword MajorTopicYN="Y">Melanocytes</Keyword>
<Keyword MajorTopicYN="Y">Mitochondria</Keyword>
<Keyword MajorTopicYN="Y">Nrf2</Keyword>
<Keyword MajorTopicYN="Y">Vitiligo</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>05</Month>
<Day>30</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2018</Year>
<Month>08</Month>
<Day>26</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2018</Year>
<Month>10</Month>
<Day>09</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2018</Year>
<Month>10</Month>
<Day>21</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2019</Year>
<Month>9</Month>
<Day>29</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2018</Year>
<Month>10</Month>
<Day>21</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
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<ArticleId IdType="doi">10.1016/j.freeradbiomed.2018.10.421</ArticleId>
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<name sortKey="Guo, Sen" sort="Guo, Sen" uniqKey="Guo S" first="Sen" last="Guo">Sen Guo</name>
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<name sortKey="Li, Chunying" sort="Li, Chunying" uniqKey="Li C" first="Chunying" last="Li">Chunying Li</name>
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	Serveur d'exploration sur les mitochondries dans l'oxydoréduction chez les plantes
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur les mitochondries dans l'oxydoréduction chez les plantes

Baicalein protects human vitiligo melanocytes from oxidative stress through activation of NF-E2-related factor2 (Nrf2) signaling pathway.

Baicalein protects human vitiligo melanocytes from oxidative stress through activation of NF-E2-related factor2 (Nrf2) signaling pathway.

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