Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression

Psoriasis vulgaris (PV) is a common inflammatory skin disorder with immune imbalance contributing to its pathology. It has been reported that auranofin, a known anti-rheumatic drug, has the therapeutic effects on inflammatory diseases. However, the effects and underlying mechanisms of auranofin on P...
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Autor*in:	Xin Luo [verfasserIn] Yuwen Su [verfasserIn] Lian Zhong [verfasserIn] Qiqi Kuang [verfasserIn] Yanshan Zhu [verfasserIn] Xiao Zhou [verfasserIn] Guishao Tang [verfasserIn] Yunfeng Fu [verfasserIn] Siying Li [verfasserIn] Ruifang Wu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Auranofin Psoriasis vulgaris Keratinocyte Fatty acid 2-hydroxylase FA2H Anti-inflammation

Übergeordnetes Werk:	In: Biomedicine & Pharmacotherapy - Elsevier, 2021, 160(2023), Seite 114421-
Übergeordnetes Werk:	volume:160 ; year:2023 ; pages:114421-

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.biopha.2023.114421

Katalog-ID:	DOAJ079846459

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520			\|a Psoriasis vulgaris (PV) is a common inflammatory skin disorder with immune imbalance contributing to its pathology. It has been reported that auranofin, a known anti-rheumatic drug, has the therapeutic effects on inflammatory diseases. However, the effects and underlying mechanisms of auranofin on PV have not been reported. Here, we showed that auranofin significantly attenuated the mixture of five proinflammatory cytokines (termed as M5) induced hyperproliferation and inflammation in HaCaT cells, a kind of human immortalized keratinocyte cell line. Topical administration of auranofin markedly alleviated the imiquimod (IMQ)-induced mouse psoriatic dermatitis both in appearance and in pathology. The psoriasis area and severity index (PASI) score, acanthosis, dermal infiltrated inflammatory cells and Ki-67 expression were improved obviously. The results of RNA-sequencing from both M5-induced HaCaT cells and IMQ-treated mouse dermatitis showed that auranofin could regulate inflammation-related signaling pathway. Meanwhile, we observed that fatty acid 2-hydroxylase (FA2H), a key molecule in lipid metabolism, was significantly increased after auraonfin treatment in both M5-induced HaCaT cells and IMQ-treated mouse skin. Knockdown of FA2H in HaCaT cells remarkably inhibited cell apoptosis, increased cell proliferation and the expression profiles of inflammatory-related genes, whereas FA2H overexpression had opposite effect. In conclusion, auranofin notably alleviated IMQ-induced psoriasis-like skin inflammation, which might be mediated by increasing FA2H expression, suggesting its potential to be a novel strategy for psoriasis treatment.
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allfields	10.1016/j.biopha.2023.114421 doi (DE-627)DOAJ079846459 (DE-599)DOAJ29a5efedf38e42db95179df806556a03 DE-627 ger DE-627 rakwb eng RM1-950 Xin Luo verfasserin aut Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Psoriasis vulgaris (PV) is a common inflammatory skin disorder with immune imbalance contributing to its pathology. It has been reported that auranofin, a known anti-rheumatic drug, has the therapeutic effects on inflammatory diseases. However, the effects and underlying mechanisms of auranofin on PV have not been reported. Here, we showed that auranofin significantly attenuated the mixture of five proinflammatory cytokines (termed as M5) induced hyperproliferation and inflammation in HaCaT cells, a kind of human immortalized keratinocyte cell line. Topical administration of auranofin markedly alleviated the imiquimod (IMQ)-induced mouse psoriatic dermatitis both in appearance and in pathology. The psoriasis area and severity index (PASI) score, acanthosis, dermal infiltrated inflammatory cells and Ki-67 expression were improved obviously. The results of RNA-sequencing from both M5-induced HaCaT cells and IMQ-treated mouse dermatitis showed that auranofin could regulate inflammation-related signaling pathway. Meanwhile, we observed that fatty acid 2-hydroxylase (FA2H), a key molecule in lipid metabolism, was significantly increased after auraonfin treatment in both M5-induced HaCaT cells and IMQ-treated mouse skin. Knockdown of FA2H in HaCaT cells remarkably inhibited cell apoptosis, increased cell proliferation and the expression profiles of inflammatory-related genes, whereas FA2H overexpression had opposite effect. In conclusion, auranofin notably alleviated IMQ-induced psoriasis-like skin inflammation, which might be mediated by increasing FA2H expression, suggesting its potential to be a novel strategy for psoriasis treatment. Auranofin Psoriasis vulgaris Keratinocyte Fatty acid 2-hydroxylase FA2H Anti-inflammation Therapeutics. Pharmacology Yuwen Su verfasserin aut Lian Zhong verfasserin aut Qiqi Kuang verfasserin aut Yanshan Zhu verfasserin aut Xiao Zhou verfasserin aut Guishao Tang verfasserin aut Yunfeng Fu verfasserin aut Siying Li verfasserin aut Ruifang Wu verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 160(2023), Seite 114421- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:160 year:2023 pages:114421- https://doi.org/10.1016/j.biopha.2023.114421 kostenfrei https://doaj.org/article/29a5efedf38e42db95179df806556a03 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332223002093 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 160 2023 114421-
spelling	10.1016/j.biopha.2023.114421 doi (DE-627)DOAJ079846459 (DE-599)DOAJ29a5efedf38e42db95179df806556a03 DE-627 ger DE-627 rakwb eng RM1-950 Xin Luo verfasserin aut Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Psoriasis vulgaris (PV) is a common inflammatory skin disorder with immune imbalance contributing to its pathology. It has been reported that auranofin, a known anti-rheumatic drug, has the therapeutic effects on inflammatory diseases. However, the effects and underlying mechanisms of auranofin on PV have not been reported. Here, we showed that auranofin significantly attenuated the mixture of five proinflammatory cytokines (termed as M5) induced hyperproliferation and inflammation in HaCaT cells, a kind of human immortalized keratinocyte cell line. Topical administration of auranofin markedly alleviated the imiquimod (IMQ)-induced mouse psoriatic dermatitis both in appearance and in pathology. The psoriasis area and severity index (PASI) score, acanthosis, dermal infiltrated inflammatory cells and Ki-67 expression were improved obviously. The results of RNA-sequencing from both M5-induced HaCaT cells and IMQ-treated mouse dermatitis showed that auranofin could regulate inflammation-related signaling pathway. Meanwhile, we observed that fatty acid 2-hydroxylase (FA2H), a key molecule in lipid metabolism, was significantly increased after auraonfin treatment in both M5-induced HaCaT cells and IMQ-treated mouse skin. Knockdown of FA2H in HaCaT cells remarkably inhibited cell apoptosis, increased cell proliferation and the expression profiles of inflammatory-related genes, whereas FA2H overexpression had opposite effect. In conclusion, auranofin notably alleviated IMQ-induced psoriasis-like skin inflammation, which might be mediated by increasing FA2H expression, suggesting its potential to be a novel strategy for psoriasis treatment. Auranofin Psoriasis vulgaris Keratinocyte Fatty acid 2-hydroxylase FA2H Anti-inflammation Therapeutics. Pharmacology Yuwen Su verfasserin aut Lian Zhong verfasserin aut Qiqi Kuang verfasserin aut Yanshan Zhu verfasserin aut Xiao Zhou verfasserin aut Guishao Tang verfasserin aut Yunfeng Fu verfasserin aut Siying Li verfasserin aut Ruifang Wu verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 160(2023), Seite 114421- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:160 year:2023 pages:114421- https://doi.org/10.1016/j.biopha.2023.114421 kostenfrei https://doaj.org/article/29a5efedf38e42db95179df806556a03 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332223002093 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 160 2023 114421-
allfields_unstemmed	10.1016/j.biopha.2023.114421 doi (DE-627)DOAJ079846459 (DE-599)DOAJ29a5efedf38e42db95179df806556a03 DE-627 ger DE-627 rakwb eng RM1-950 Xin Luo verfasserin aut Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Psoriasis vulgaris (PV) is a common inflammatory skin disorder with immune imbalance contributing to its pathology. It has been reported that auranofin, a known anti-rheumatic drug, has the therapeutic effects on inflammatory diseases. However, the effects and underlying mechanisms of auranofin on PV have not been reported. Here, we showed that auranofin significantly attenuated the mixture of five proinflammatory cytokines (termed as M5) induced hyperproliferation and inflammation in HaCaT cells, a kind of human immortalized keratinocyte cell line. Topical administration of auranofin markedly alleviated the imiquimod (IMQ)-induced mouse psoriatic dermatitis both in appearance and in pathology. The psoriasis area and severity index (PASI) score, acanthosis, dermal infiltrated inflammatory cells and Ki-67 expression were improved obviously. The results of RNA-sequencing from both M5-induced HaCaT cells and IMQ-treated mouse dermatitis showed that auranofin could regulate inflammation-related signaling pathway. Meanwhile, we observed that fatty acid 2-hydroxylase (FA2H), a key molecule in lipid metabolism, was significantly increased after auraonfin treatment in both M5-induced HaCaT cells and IMQ-treated mouse skin. Knockdown of FA2H in HaCaT cells remarkably inhibited cell apoptosis, increased cell proliferation and the expression profiles of inflammatory-related genes, whereas FA2H overexpression had opposite effect. In conclusion, auranofin notably alleviated IMQ-induced psoriasis-like skin inflammation, which might be mediated by increasing FA2H expression, suggesting its potential to be a novel strategy for psoriasis treatment. Auranofin Psoriasis vulgaris Keratinocyte Fatty acid 2-hydroxylase FA2H Anti-inflammation Therapeutics. Pharmacology Yuwen Su verfasserin aut Lian Zhong verfasserin aut Qiqi Kuang verfasserin aut Yanshan Zhu verfasserin aut Xiao Zhou verfasserin aut Guishao Tang verfasserin aut Yunfeng Fu verfasserin aut Siying Li verfasserin aut Ruifang Wu verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 160(2023), Seite 114421- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:160 year:2023 pages:114421- https://doi.org/10.1016/j.biopha.2023.114421 kostenfrei https://doaj.org/article/29a5efedf38e42db95179df806556a03 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332223002093 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 160 2023 114421-
allfieldsGer	10.1016/j.biopha.2023.114421 doi (DE-627)DOAJ079846459 (DE-599)DOAJ29a5efedf38e42db95179df806556a03 DE-627 ger DE-627 rakwb eng RM1-950 Xin Luo verfasserin aut Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Psoriasis vulgaris (PV) is a common inflammatory skin disorder with immune imbalance contributing to its pathology. It has been reported that auranofin, a known anti-rheumatic drug, has the therapeutic effects on inflammatory diseases. However, the effects and underlying mechanisms of auranofin on PV have not been reported. Here, we showed that auranofin significantly attenuated the mixture of five proinflammatory cytokines (termed as M5) induced hyperproliferation and inflammation in HaCaT cells, a kind of human immortalized keratinocyte cell line. Topical administration of auranofin markedly alleviated the imiquimod (IMQ)-induced mouse psoriatic dermatitis both in appearance and in pathology. The psoriasis area and severity index (PASI) score, acanthosis, dermal infiltrated inflammatory cells and Ki-67 expression were improved obviously. The results of RNA-sequencing from both M5-induced HaCaT cells and IMQ-treated mouse dermatitis showed that auranofin could regulate inflammation-related signaling pathway. Meanwhile, we observed that fatty acid 2-hydroxylase (FA2H), a key molecule in lipid metabolism, was significantly increased after auraonfin treatment in both M5-induced HaCaT cells and IMQ-treated mouse skin. Knockdown of FA2H in HaCaT cells remarkably inhibited cell apoptosis, increased cell proliferation and the expression profiles of inflammatory-related genes, whereas FA2H overexpression had opposite effect. In conclusion, auranofin notably alleviated IMQ-induced psoriasis-like skin inflammation, which might be mediated by increasing FA2H expression, suggesting its potential to be a novel strategy for psoriasis treatment. Auranofin Psoriasis vulgaris Keratinocyte Fatty acid 2-hydroxylase FA2H Anti-inflammation Therapeutics. Pharmacology Yuwen Su verfasserin aut Lian Zhong verfasserin aut Qiqi Kuang verfasserin aut Yanshan Zhu verfasserin aut Xiao Zhou verfasserin aut Guishao Tang verfasserin aut Yunfeng Fu verfasserin aut Siying Li verfasserin aut Ruifang Wu verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 160(2023), Seite 114421- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:160 year:2023 pages:114421- https://doi.org/10.1016/j.biopha.2023.114421 kostenfrei https://doaj.org/article/29a5efedf38e42db95179df806556a03 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332223002093 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 160 2023 114421-
allfieldsSound	10.1016/j.biopha.2023.114421 doi (DE-627)DOAJ079846459 (DE-599)DOAJ29a5efedf38e42db95179df806556a03 DE-627 ger DE-627 rakwb eng RM1-950 Xin Luo verfasserin aut Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Psoriasis vulgaris (PV) is a common inflammatory skin disorder with immune imbalance contributing to its pathology. It has been reported that auranofin, a known anti-rheumatic drug, has the therapeutic effects on inflammatory diseases. However, the effects and underlying mechanisms of auranofin on PV have not been reported. Here, we showed that auranofin significantly attenuated the mixture of five proinflammatory cytokines (termed as M5) induced hyperproliferation and inflammation in HaCaT cells, a kind of human immortalized keratinocyte cell line. Topical administration of auranofin markedly alleviated the imiquimod (IMQ)-induced mouse psoriatic dermatitis both in appearance and in pathology. The psoriasis area and severity index (PASI) score, acanthosis, dermal infiltrated inflammatory cells and Ki-67 expression were improved obviously. The results of RNA-sequencing from both M5-induced HaCaT cells and IMQ-treated mouse dermatitis showed that auranofin could regulate inflammation-related signaling pathway. Meanwhile, we observed that fatty acid 2-hydroxylase (FA2H), a key molecule in lipid metabolism, was significantly increased after auraonfin treatment in both M5-induced HaCaT cells and IMQ-treated mouse skin. Knockdown of FA2H in HaCaT cells remarkably inhibited cell apoptosis, increased cell proliferation and the expression profiles of inflammatory-related genes, whereas FA2H overexpression had opposite effect. In conclusion, auranofin notably alleviated IMQ-induced psoriasis-like skin inflammation, which might be mediated by increasing FA2H expression, suggesting its potential to be a novel strategy for psoriasis treatment. Auranofin Psoriasis vulgaris Keratinocyte Fatty acid 2-hydroxylase FA2H Anti-inflammation Therapeutics. Pharmacology Yuwen Su verfasserin aut Lian Zhong verfasserin aut Qiqi Kuang verfasserin aut Yanshan Zhu verfasserin aut Xiao Zhou verfasserin aut Guishao Tang verfasserin aut Yunfeng Fu verfasserin aut Siying Li verfasserin aut Ruifang Wu verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 160(2023), Seite 114421- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:160 year:2023 pages:114421- https://doi.org/10.1016/j.biopha.2023.114421 kostenfrei https://doaj.org/article/29a5efedf38e42db95179df806556a03 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332223002093 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 160 2023 114421-
language	English
source	In Biomedicine & Pharmacotherapy 160(2023), Seite 114421- volume:160 year:2023 pages:114421-
sourceStr	In Biomedicine & Pharmacotherapy 160(2023), Seite 114421- volume:160 year:2023 pages:114421-
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Auranofin Psoriasis vulgaris Keratinocyte Fatty acid 2-hydroxylase FA2H Anti-inflammation Therapeutics. Pharmacology
isfreeaccess_bool	true
container_title	Biomedicine & Pharmacotherapy
authorswithroles_txt_mv	Xin Luo @@aut@@ Yuwen Su @@aut@@ Lian Zhong @@aut@@ Qiqi Kuang @@aut@@ Yanshan Zhu @@aut@@ Xiao Zhou @@aut@@ Guishao Tang @@aut@@ Yunfeng Fu @@aut@@ Siying Li @@aut@@ Ruifang Wu @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	306717565
id	DOAJ079846459
language_de	englisch
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callnumber-first	R - Medicine
author	Xin Luo
spellingShingle	Xin Luo misc RM1-950 misc Auranofin misc Psoriasis vulgaris misc Keratinocyte misc Fatty acid 2-hydroxylase misc FA2H misc Anti-inflammation misc Therapeutics. Pharmacology Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression
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topic_title	RM1-950 Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression Auranofin Psoriasis vulgaris Keratinocyte Fatty acid 2-hydroxylase FA2H Anti-inflammation
topic	misc RM1-950 misc Auranofin misc Psoriasis vulgaris misc Keratinocyte misc Fatty acid 2-hydroxylase misc FA2H misc Anti-inflammation misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc Auranofin misc Psoriasis vulgaris misc Keratinocyte misc Fatty acid 2-hydroxylase misc FA2H misc Anti-inflammation misc Therapeutics. Pharmacology
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title	Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression
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title_full	Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression
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author_browse	Xin Luo Yuwen Su Lian Zhong Qiqi Kuang Yanshan Zhu Xiao Zhou Guishao Tang Yunfeng Fu Siying Li Ruifang Wu
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title_sort	auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating fa2h expression
callnumber	RM1-950
title_auth	Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression
abstract	Psoriasis vulgaris (PV) is a common inflammatory skin disorder with immune imbalance contributing to its pathology. It has been reported that auranofin, a known anti-rheumatic drug, has the therapeutic effects on inflammatory diseases. However, the effects and underlying mechanisms of auranofin on PV have not been reported. Here, we showed that auranofin significantly attenuated the mixture of five proinflammatory cytokines (termed as M5) induced hyperproliferation and inflammation in HaCaT cells, a kind of human immortalized keratinocyte cell line. Topical administration of auranofin markedly alleviated the imiquimod (IMQ)-induced mouse psoriatic dermatitis both in appearance and in pathology. The psoriasis area and severity index (PASI) score, acanthosis, dermal infiltrated inflammatory cells and Ki-67 expression were improved obviously. The results of RNA-sequencing from both M5-induced HaCaT cells and IMQ-treated mouse dermatitis showed that auranofin could regulate inflammation-related signaling pathway. Meanwhile, we observed that fatty acid 2-hydroxylase (FA2H), a key molecule in lipid metabolism, was significantly increased after auraonfin treatment in both M5-induced HaCaT cells and IMQ-treated mouse skin. Knockdown of FA2H in HaCaT cells remarkably inhibited cell apoptosis, increased cell proliferation and the expression profiles of inflammatory-related genes, whereas FA2H overexpression had opposite effect. In conclusion, auranofin notably alleviated IMQ-induced psoriasis-like skin inflammation, which might be mediated by increasing FA2H expression, suggesting its potential to be a novel strategy for psoriasis treatment.
abstractGer	Psoriasis vulgaris (PV) is a common inflammatory skin disorder with immune imbalance contributing to its pathology. It has been reported that auranofin, a known anti-rheumatic drug, has the therapeutic effects on inflammatory diseases. However, the effects and underlying mechanisms of auranofin on PV have not been reported. Here, we showed that auranofin significantly attenuated the mixture of five proinflammatory cytokines (termed as M5) induced hyperproliferation and inflammation in HaCaT cells, a kind of human immortalized keratinocyte cell line. Topical administration of auranofin markedly alleviated the imiquimod (IMQ)-induced mouse psoriatic dermatitis both in appearance and in pathology. The psoriasis area and severity index (PASI) score, acanthosis, dermal infiltrated inflammatory cells and Ki-67 expression were improved obviously. The results of RNA-sequencing from both M5-induced HaCaT cells and IMQ-treated mouse dermatitis showed that auranofin could regulate inflammation-related signaling pathway. Meanwhile, we observed that fatty acid 2-hydroxylase (FA2H), a key molecule in lipid metabolism, was significantly increased after auraonfin treatment in both M5-induced HaCaT cells and IMQ-treated mouse skin. Knockdown of FA2H in HaCaT cells remarkably inhibited cell apoptosis, increased cell proliferation and the expression profiles of inflammatory-related genes, whereas FA2H overexpression had opposite effect. In conclusion, auranofin notably alleviated IMQ-induced psoriasis-like skin inflammation, which might be mediated by increasing FA2H expression, suggesting its potential to be a novel strategy for psoriasis treatment.
abstract_unstemmed	Psoriasis vulgaris (PV) is a common inflammatory skin disorder with immune imbalance contributing to its pathology. It has been reported that auranofin, a known anti-rheumatic drug, has the therapeutic effects on inflammatory diseases. However, the effects and underlying mechanisms of auranofin on PV have not been reported. Here, we showed that auranofin significantly attenuated the mixture of five proinflammatory cytokines (termed as M5) induced hyperproliferation and inflammation in HaCaT cells, a kind of human immortalized keratinocyte cell line. Topical administration of auranofin markedly alleviated the imiquimod (IMQ)-induced mouse psoriatic dermatitis both in appearance and in pathology. The psoriasis area and severity index (PASI) score, acanthosis, dermal infiltrated inflammatory cells and Ki-67 expression were improved obviously. The results of RNA-sequencing from both M5-induced HaCaT cells and IMQ-treated mouse dermatitis showed that auranofin could regulate inflammation-related signaling pathway. Meanwhile, we observed that fatty acid 2-hydroxylase (FA2H), a key molecule in lipid metabolism, was significantly increased after auraonfin treatment in both M5-induced HaCaT cells and IMQ-treated mouse skin. Knockdown of FA2H in HaCaT cells remarkably inhibited cell apoptosis, increased cell proliferation and the expression profiles of inflammatory-related genes, whereas FA2H overexpression had opposite effect. In conclusion, auranofin notably alleviated IMQ-induced psoriasis-like skin inflammation, which might be mediated by increasing FA2H expression, suggesting its potential to be a novel strategy for psoriasis treatment.
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title_short	Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression
url	https://doi.org/10.1016/j.biopha.2023.114421 https://doaj.org/article/29a5efedf38e42db95179df806556a03 http://www.sciencedirect.com/science/article/pii/S0753332223002093 https://doaj.org/toc/0753-3322
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Auranofin ameliorates psoriasis-like dermatitis in an imiquimod-induced mouse by inhibiting of inflammation and upregulating FA2H expression

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