Puerarin Reduces Oxidative Damage and Photoaging Caused by UVA Radiation in Human Fibroblasts by Regulating Nrf2 and MAPK Signaling Pathways
Fibroblasts account for more than 95% of dermal cells maintaining dermal structure and function. However, UVA penetrates the dermis and causes oxidative stress that damages the dermis and accelerates skin aging. Puerarin, the main active ingredient of , has been demonstrated to withstand oxidative s...
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| Veröffentlicht in: | Nutrients 2022-11, Vol.14 (22), p.4724 |
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| creator | Mo, Qiuting Li, Shuping You, Shiquan Wang, Dongdong Zhang, Jiachan Li, Meng Wang, Changtao |
| description | Fibroblasts account for more than 95% of dermal cells maintaining dermal structure and function. However, UVA penetrates the dermis and causes oxidative stress that damages the dermis and accelerates skin aging. Puerarin, the main active ingredient of
, has been demonstrated to withstand oxidative stress caused by a variety of factors. However, there are limited findings on whether puerarin protects fibroblasts from UVA-induced oxidative stress damage. The effects of puerarin on human skin fibroblasts (HSF) under UVA-induced oxidative stress were investigated in this study. It is found that puerarin upregulates antioxidant enzymes' mRNA expression level and their content through modulating the KEAP1-Nrf2/ARE signaling pathway, thus improving cell antioxidant capacity and successfully eliminating UVA-induced reactive oxygen species (ROS) and lipid oxidation product malondialdehyde (MDA). Additionally, puerarin blocks the overexpression of human extracellular signal-regulated kinase (ERK), human c-Jun amino-terminal kinase (JNK), and P38, which downregulates matrix metalloproteinase 1 (MMP-1) expression and increases type I collagen (COL-1) expression. Moreover, preliminary research on mouse skin suggests that puerarin can hydrate, moisturize, and increase the antioxidant capacity of skin tissue. These findings suggest that puerarin can protect the skin against photoaging. |
| doi_str_mv | 10.3390/nu14224724 |
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, has been demonstrated to withstand oxidative stress caused by a variety of factors. However, there are limited findings on whether puerarin protects fibroblasts from UVA-induced oxidative stress damage. The effects of puerarin on human skin fibroblasts (HSF) under UVA-induced oxidative stress were investigated in this study. It is found that puerarin upregulates antioxidant enzymes' mRNA expression level and their content through modulating the KEAP1-Nrf2/ARE signaling pathway, thus improving cell antioxidant capacity and successfully eliminating UVA-induced reactive oxygen species (ROS) and lipid oxidation product malondialdehyde (MDA). Additionally, puerarin blocks the overexpression of human extracellular signal-regulated kinase (ERK), human c-Jun amino-terminal kinase (JNK), and P38, which downregulates matrix metalloproteinase 1 (MMP-1) expression and increases type I collagen (COL-1) expression. Moreover, preliminary research on mouse skin suggests that puerarin can hydrate, moisturize, and increase the antioxidant capacity of skin tissue. These findings suggest that puerarin can protect the skin against photoaging.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu14224724</identifier><identifier>PMID: 36432411</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Aging ; Angina pectoris ; Animals ; Antioxidants ; Antioxidants - metabolism ; Antioxidants - pharmacology ; Care and treatment ; Cell culture ; Collagen ; Collagen (type I) ; Dehydrogenases ; Dermis ; Enzymes ; Extracellular signal-regulated kinase ; Fibroblasts ; Gene expression ; Humans ; Interstitial collagenase ; Kelch-Like ECH-Associated Protein 1 - genetics ; Kelch-Like ECH-Associated Protein 1 - metabolism ; Laboratory animals ; Lipid peroxidation ; Lipids ; MAP kinase ; Matrix metalloproteinase ; Matrix metalloproteinases ; Metalloproteinase ; Mice ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; Oxidation ; Oxidative Stress ; Proteins ; Radiation ; Radiation damage ; Reactive oxygen species ; RNA ; Signal Transduction ; Skin ; Skin Aging ; Structure-function relationships ; Transcription factors</subject><ispartof>Nutrients, 2022-11, Vol.14 (22), p.4724</ispartof><rights>COPYRIGHT 2022 MDPI AG</rights><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c473t-3768c253f6729110a4734f71dc9e0d7603380625214a2bf9ea3d47176a5da1ea3</citedby><cites>FETCH-LOGICAL-c473t-3768c253f6729110a4734f71dc9e0d7603380625214a2bf9ea3d47176a5da1ea3</cites><orcidid>0000-0002-7354-6480 ; 0000-0003-3990-0471</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9694396/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9694396/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36432411$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mo, Qiuting</creatorcontrib><creatorcontrib>Li, Shuping</creatorcontrib><creatorcontrib>You, Shiquan</creatorcontrib><creatorcontrib>Wang, Dongdong</creatorcontrib><creatorcontrib>Zhang, Jiachan</creatorcontrib><creatorcontrib>Li, Meng</creatorcontrib><creatorcontrib>Wang, Changtao</creatorcontrib><title>Puerarin Reduces Oxidative Damage and Photoaging Caused by UVA Radiation in Human Fibroblasts by Regulating Nrf2 and MAPK Signaling Pathways</title><title>Nutrients</title><addtitle>Nutrients</addtitle><description>Fibroblasts account for more than 95% of dermal cells maintaining dermal structure and function. However, UVA penetrates the dermis and causes oxidative stress that damages the dermis and accelerates skin aging. Puerarin, the main active ingredient of
, has been demonstrated to withstand oxidative stress caused by a variety of factors. However, there are limited findings on whether puerarin protects fibroblasts from UVA-induced oxidative stress damage. The effects of puerarin on human skin fibroblasts (HSF) under UVA-induced oxidative stress were investigated in this study. It is found that puerarin upregulates antioxidant enzymes' mRNA expression level and their content through modulating the KEAP1-Nrf2/ARE signaling pathway, thus improving cell antioxidant capacity and successfully eliminating UVA-induced reactive oxygen species (ROS) and lipid oxidation product malondialdehyde (MDA). Additionally, puerarin blocks the overexpression of human extracellular signal-regulated kinase (ERK), human c-Jun amino-terminal kinase (JNK), and P38, which downregulates matrix metalloproteinase 1 (MMP-1) expression and increases type I collagen (COL-1) expression. Moreover, preliminary research on mouse skin suggests that puerarin can hydrate, moisturize, and increase the antioxidant capacity of skin tissue. These findings suggest that puerarin can protect the skin against photoaging.</description><subject>Aging</subject><subject>Angina pectoris</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Antioxidants - pharmacology</subject><subject>Care and treatment</subject><subject>Cell culture</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Dehydrogenases</subject><subject>Dermis</subject><subject>Enzymes</subject><subject>Extracellular signal-regulated kinase</subject><subject>Fibroblasts</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Interstitial collagenase</subject><subject>Kelch-Like ECH-Associated Protein 1 - genetics</subject><subject>Kelch-Like ECH-Associated Protein 1 - metabolism</subject><subject>Laboratory animals</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>MAP kinase</subject><subject>Matrix metalloproteinase</subject><subject>Matrix metalloproteinases</subject><subject>Metalloproteinase</subject><subject>Mice</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Oxidation</subject><subject>Oxidative Stress</subject><subject>Proteins</subject><subject>Radiation</subject><subject>Radiation damage</subject><subject>Reactive oxygen species</subject><subject>RNA</subject><subject>Signal Transduction</subject><subject>Skin</subject><subject>Skin Aging</subject><subject>Structure-function relationships</subject><subject>Transcription factors</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkl1vFCEUhidGY5vaG3-AIfHGmGzla2DnxmSz2tZY7Wa13pIzAzNLMwMtDLX7H_zRMrb2wwgXHF6e88IhpyheEnzAWIXfuUQ4pVxS_qTYpVjSmRCcPX0Q7xT7MZ7jaUgsBXte7LAsU07IbvFrlUyAYB1aG50aE9HptdUw2iuDPsAAnUHgNFpt_Oihs65DS0jRaFRv0dmPBVqDtpn2DmWL4zSAQ4e2Dr7uIY5xotamS31GcurX0NI_dl8Wq8_om-0c9JO-gnHzE7bxRfGshT6a_dt1rzg7_Ph9eTw7OT36tFyczBou2ThjUswbWrJWSFoRgiGrvJVEN5XBWgrM2BwLWlLCgdZtZYBpLokUUGogebdXvL_xvUj1YHRj3BigVxfBDhC2yoNVj0-c3ajOX6lKVJxVIhu8uTUI_jKZOKrBxsb0PTjjU1RUclwSPMfzjL7-Bz33KeTCJ4pVPL8d43uqg94o61qf720mU7WQXDBaYlJm6uA_VJ7aDLbxzrQ2648S3t4kNMHHGEx7VyPBamofdd8-GX718Ffu0L_Nwn4Dk0-9lw</recordid><startdate>20221109</startdate><enddate>20221109</enddate><creator>Mo, Qiuting</creator><creator>Li, Shuping</creator><creator>You, Shiquan</creator><creator>Wang, Dongdong</creator><creator>Zhang, Jiachan</creator><creator>Li, Meng</creator><creator>Wang, Changtao</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7354-6480</orcidid><orcidid>https://orcid.org/0000-0003-3990-0471</orcidid></search><sort><creationdate>20221109</creationdate><title>Puerarin Reduces Oxidative Damage and Photoaging Caused by UVA Radiation in Human Fibroblasts by Regulating Nrf2 and MAPK Signaling Pathways</title><author>Mo, Qiuting ; 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However, UVA penetrates the dermis and causes oxidative stress that damages the dermis and accelerates skin aging. Puerarin, the main active ingredient of
, has been demonstrated to withstand oxidative stress caused by a variety of factors. However, there are limited findings on whether puerarin protects fibroblasts from UVA-induced oxidative stress damage. The effects of puerarin on human skin fibroblasts (HSF) under UVA-induced oxidative stress were investigated in this study. It is found that puerarin upregulates antioxidant enzymes' mRNA expression level and their content through modulating the KEAP1-Nrf2/ARE signaling pathway, thus improving cell antioxidant capacity and successfully eliminating UVA-induced reactive oxygen species (ROS) and lipid oxidation product malondialdehyde (MDA). Additionally, puerarin blocks the overexpression of human extracellular signal-regulated kinase (ERK), human c-Jun amino-terminal kinase (JNK), and P38, which downregulates matrix metalloproteinase 1 (MMP-1) expression and increases type I collagen (COL-1) expression. Moreover, preliminary research on mouse skin suggests that puerarin can hydrate, moisturize, and increase the antioxidant capacity of skin tissue. These findings suggest that puerarin can protect the skin against photoaging.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36432411</pmid><doi>10.3390/nu14224724</doi><orcidid>https://orcid.org/0000-0002-7354-6480</orcidid><orcidid>https://orcid.org/0000-0003-3990-0471</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | Aging Angina pectoris Animals Antioxidants Antioxidants - metabolism Antioxidants - pharmacology Care and treatment Cell culture Collagen Collagen (type I) Dehydrogenases Dermis Enzymes Extracellular signal-regulated kinase Fibroblasts Gene expression Humans Interstitial collagenase Kelch-Like ECH-Associated Protein 1 - genetics Kelch-Like ECH-Associated Protein 1 - metabolism Laboratory animals Lipid peroxidation Lipids MAP kinase Matrix metalloproteinase Matrix metalloproteinases Metalloproteinase Mice NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism Oxidation Oxidative Stress Proteins Radiation Radiation damage Reactive oxygen species RNA Signal Transduction Skin Skin Aging Structure-function relationships Transcription factors |
| title | Puerarin Reduces Oxidative Damage and Photoaging Caused by UVA Radiation in Human Fibroblasts by Regulating Nrf2 and MAPK Signaling Pathways |
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