Resveratrol Alleviates Diabetic Periodontitis-Induced Alveolar Osteocyte Ferroptosis Possibly via Regulation of SLC7A11/GPX4
The mode and mechanism of diabetic periodontitis-induced alveolar-osteocyte death are still unclear. This study aimed to investigate the occurrence of ferroptosis in alveolar osteocytes during diabetic periodontitis and the therapeutic potential of resveratrol to alleviate osteocyte ferroptosis. Dia...
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| Veröffentlicht in: | Nutrients 2023-04, Vol.15 (9), p.2115 |
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| description | The mode and mechanism of diabetic periodontitis-induced alveolar-osteocyte death are still unclear. This study aimed to investigate the occurrence of ferroptosis in alveolar osteocytes during diabetic periodontitis and the therapeutic potential of resveratrol to alleviate osteocyte ferroptosis. Diabetic periodontitis was induced in C57/BL6-male mice and treated with or without resveratrol. Periodontitis pathogenicity was analyzed by micro-CT and histology, and alveolar-osteocyte ferroptosis was analyzed by immunohistochemistry. MLOY4 osteocytes were treated with
-derived lipopolysaccharide (LPS)+advanced glycosylated end products (AGEs) mimicking diabetic periodontitis condition in vitro, with or without resveratrol or ferrostatin-1 (ferroptosis inhibitor). Osteocyte ferroptosis and expression of inflammatory mediators were analyzed. Diabetic periodontitis aggravated periodontitis pathogenicity and inhibited the expression of GPX4 and SLC7A11 in alveolar osteocytes and resveratrol alleviated these effects. LPS+AGEs triggered osteocyte ferroptosis in vitro as indicated by the downregulated GPX4 and SLC7A11, upregulated malondialdehyde, disrupted mitochondrial morphology, and overexpressed pro-inflammatory mediators IL-1β, TNF-α, SOST, RANKL, and IL-6, and ferrostatin-1 or resveratrol treatment reversed these effects. LPS+AGEs upregulated pIKBα and pNF-κB p65 expression in osteocytes, and resveratrol or ferrostatin-1 reversed this effect. In conclusion, diabetic periodontitis triggers alveolar osteocyte ferroptosis possibly via disruption of the SLC7A11/GPX4 axis, and resveratrol has therapeutic potential to correct this biological event. |
| doi_str_mv | 10.3390/nu15092115 |
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| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10181281</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A749233205</galeid><sourcerecordid>A749233205</sourcerecordid><originalsourceid>FETCH-LOGICAL-c474t-5667ce90ee92a911afa40337bdb9b19865d0c9fe9281e494656ec0c5eef8dfa13</originalsourceid><addsrcrecordid>eNptkltrHCEUgIfS0oQ0L_0BRehLKUziZUbHp7JsmgssZElb6Js4zpmtwdWtOgsL_fF1yb1UHxTPdz45eqrqPcEnjEl86ifSYkkJaV9VhxQLWnPesNfP9gfVcUq3eD8EFpy9rQ6YaBilQhxWf24gbSHqHINDM-dga3WGhM6s7iFbg5YQbRiCzzbbVF_5YTIwFHILwemIrlOGYHYZ0DnEGDY5JJvQMqRke7dDxYZuYDU5nW3wKIzo22IuZoScXix_Nu-qN6N2CY7v16Pqx_nX7_PLenF9cTWfLWrTiCbXLefCgMQAkmpJiB51gxkT_dDLnsiOtwM2cizRjkAjG95yMNi0AGM3jJqwo-rLnXcz9WsYDPgctVObaNc67lTQVr2MePtLrcJWEUw6UqzF8OneEMPvCVJWa5sMOKc9hCkp2jFOpWjbtqAf_0FvwxR9qa9QhArCOyaeqJV2oKwfQ7nY7KVqJhpJGaN47zr5D1XmAGtrgofRlvMXCZ_vEkwsXxBhfCySYLXvF_XULwX-8PxZHtGH7mB_AXDwuqY</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2812716837</pqid></control><display><type>article</type><title>Resveratrol Alleviates Diabetic Periodontitis-Induced Alveolar Osteocyte Ferroptosis Possibly via Regulation of SLC7A11/GPX4</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><creator>Li, Yue ; Huang, Zhijun ; Pan, Shuaifei ; Feng, Yuhui ; He, Haokun ; Cheng, Shuguang ; Wang, Lijing ; Wang, Liping ; Pathak, Janak Lal</creator><creatorcontrib>Li, Yue ; Huang, Zhijun ; Pan, Shuaifei ; Feng, Yuhui ; He, Haokun ; Cheng, Shuguang ; Wang, Lijing ; Wang, Liping ; Pathak, Janak Lal</creatorcontrib><description>The mode and mechanism of diabetic periodontitis-induced alveolar-osteocyte death are still unclear. This study aimed to investigate the occurrence of ferroptosis in alveolar osteocytes during diabetic periodontitis and the therapeutic potential of resveratrol to alleviate osteocyte ferroptosis. Diabetic periodontitis was induced in C57/BL6-male mice and treated with or without resveratrol. Periodontitis pathogenicity was analyzed by micro-CT and histology, and alveolar-osteocyte ferroptosis was analyzed by immunohistochemistry. MLOY4 osteocytes were treated with
-derived lipopolysaccharide (LPS)+advanced glycosylated end products (AGEs) mimicking diabetic periodontitis condition in vitro, with or without resveratrol or ferrostatin-1 (ferroptosis inhibitor). Osteocyte ferroptosis and expression of inflammatory mediators were analyzed. Diabetic periodontitis aggravated periodontitis pathogenicity and inhibited the expression of GPX4 and SLC7A11 in alveolar osteocytes and resveratrol alleviated these effects. LPS+AGEs triggered osteocyte ferroptosis in vitro as indicated by the downregulated GPX4 and SLC7A11, upregulated malondialdehyde, disrupted mitochondrial morphology, and overexpressed pro-inflammatory mediators IL-1β, TNF-α, SOST, RANKL, and IL-6, and ferrostatin-1 or resveratrol treatment reversed these effects. LPS+AGEs upregulated pIKBα and pNF-κB p65 expression in osteocytes, and resveratrol or ferrostatin-1 reversed this effect. In conclusion, diabetic periodontitis triggers alveolar osteocyte ferroptosis possibly via disruption of the SLC7A11/GPX4 axis, and resveratrol has therapeutic potential to correct this biological event.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu15092115</identifier><identifier>PMID: 37432277</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Age ; Alveoli ; Apoptosis ; Cell culture ; Computed tomography ; Diabetes ; Diabetes mellitus ; Ethylenediaminetetraacetic acid ; Ferroptosis ; Gum disease ; Health aspects ; Histology ; Homeostasis ; Immunohistochemistry ; Inflammation ; Interleukin 6 ; Lipid peroxidation ; Lipids ; Lipopolysaccharides ; Mitochondria ; Osteocytes ; Osteoporosis ; Pathogenicity ; Pathogens ; Periodontitis ; Proteins ; Resveratrol ; SOST protein ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>Nutrients, 2023-04, Vol.15 (9), p.2115</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 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>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-5667ce90ee92a911afa40337bdb9b19865d0c9fe9281e494656ec0c5eef8dfa13</citedby><cites>FETCH-LOGICAL-c474t-5667ce90ee92a911afa40337bdb9b19865d0c9fe9281e494656ec0c5eef8dfa13</cites><orcidid>0000-0003-2576-443X</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/PMC10181281/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10181281/$$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/37432277$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Yue</creatorcontrib><creatorcontrib>Huang, Zhijun</creatorcontrib><creatorcontrib>Pan, Shuaifei</creatorcontrib><creatorcontrib>Feng, Yuhui</creatorcontrib><creatorcontrib>He, Haokun</creatorcontrib><creatorcontrib>Cheng, Shuguang</creatorcontrib><creatorcontrib>Wang, Lijing</creatorcontrib><creatorcontrib>Wang, Liping</creatorcontrib><creatorcontrib>Pathak, Janak Lal</creatorcontrib><title>Resveratrol Alleviates Diabetic Periodontitis-Induced Alveolar Osteocyte Ferroptosis Possibly via Regulation of SLC7A11/GPX4</title><title>Nutrients</title><addtitle>Nutrients</addtitle><description>The mode and mechanism of diabetic periodontitis-induced alveolar-osteocyte death are still unclear. This study aimed to investigate the occurrence of ferroptosis in alveolar osteocytes during diabetic periodontitis and the therapeutic potential of resveratrol to alleviate osteocyte ferroptosis. Diabetic periodontitis was induced in C57/BL6-male mice and treated with or without resveratrol. Periodontitis pathogenicity was analyzed by micro-CT and histology, and alveolar-osteocyte ferroptosis was analyzed by immunohistochemistry. MLOY4 osteocytes were treated with
-derived lipopolysaccharide (LPS)+advanced glycosylated end products (AGEs) mimicking diabetic periodontitis condition in vitro, with or without resveratrol or ferrostatin-1 (ferroptosis inhibitor). Osteocyte ferroptosis and expression of inflammatory mediators were analyzed. Diabetic periodontitis aggravated periodontitis pathogenicity and inhibited the expression of GPX4 and SLC7A11 in alveolar osteocytes and resveratrol alleviated these effects. LPS+AGEs triggered osteocyte ferroptosis in vitro as indicated by the downregulated GPX4 and SLC7A11, upregulated malondialdehyde, disrupted mitochondrial morphology, and overexpressed pro-inflammatory mediators IL-1β, TNF-α, SOST, RANKL, and IL-6, and ferrostatin-1 or resveratrol treatment reversed these effects. LPS+AGEs upregulated pIKBα and pNF-κB p65 expression in osteocytes, and resveratrol or ferrostatin-1 reversed this effect. In conclusion, diabetic periodontitis triggers alveolar osteocyte ferroptosis possibly via disruption of the SLC7A11/GPX4 axis, and resveratrol has therapeutic potential to correct this biological event.</description><subject>Age</subject><subject>Alveoli</subject><subject>Apoptosis</subject><subject>Cell culture</subject><subject>Computed tomography</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Ferroptosis</subject><subject>Gum disease</subject><subject>Health aspects</subject><subject>Histology</subject><subject>Homeostasis</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Lipopolysaccharides</subject><subject>Mitochondria</subject><subject>Osteocytes</subject><subject>Osteoporosis</subject><subject>Pathogenicity</subject><subject>Pathogens</subject><subject>Periodontitis</subject><subject>Proteins</subject><subject>Resveratrol</subject><subject>SOST protein</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkltrHCEUgIfS0oQ0L_0BRehLKUziZUbHp7JsmgssZElb6Js4zpmtwdWtOgsL_fF1yb1UHxTPdz45eqrqPcEnjEl86ifSYkkJaV9VhxQLWnPesNfP9gfVcUq3eD8EFpy9rQ6YaBilQhxWf24gbSHqHINDM-dga3WGhM6s7iFbg5YQbRiCzzbbVF_5YTIwFHILwemIrlOGYHYZ0DnEGDY5JJvQMqRke7dDxYZuYDU5nW3wKIzo22IuZoScXix_Nu-qN6N2CY7v16Pqx_nX7_PLenF9cTWfLWrTiCbXLefCgMQAkmpJiB51gxkT_dDLnsiOtwM2cizRjkAjG95yMNi0AGM3jJqwo-rLnXcz9WsYDPgctVObaNc67lTQVr2MePtLrcJWEUw6UqzF8OneEMPvCVJWa5sMOKc9hCkp2jFOpWjbtqAf_0FvwxR9qa9QhArCOyaeqJV2oKwfQ7nY7KVqJhpJGaN47zr5D1XmAGtrgofRlvMXCZ_vEkwsXxBhfCySYLXvF_XULwX-8PxZHtGH7mB_AXDwuqY</recordid><startdate>20230428</startdate><enddate>20230428</enddate><creator>Li, Yue</creator><creator>Huang, Zhijun</creator><creator>Pan, Shuaifei</creator><creator>Feng, Yuhui</creator><creator>He, Haokun</creator><creator>Cheng, Shuguang</creator><creator>Wang, Lijing</creator><creator>Wang, Liping</creator><creator>Pathak, Janak Lal</creator><general>MDPI AG</general><general>MDPI</general><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/0000-0003-2576-443X</orcidid></search><sort><creationdate>20230428</creationdate><title>Resveratrol Alleviates Diabetic Periodontitis-Induced Alveolar Osteocyte Ferroptosis Possibly via Regulation of SLC7A11/GPX4</title><author>Li, Yue ; Huang, Zhijun ; Pan, Shuaifei ; Feng, Yuhui ; He, Haokun ; Cheng, Shuguang ; Wang, Lijing ; Wang, Liping ; Pathak, Janak Lal</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-5667ce90ee92a911afa40337bdb9b19865d0c9fe9281e494656ec0c5eef8dfa13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Age</topic><topic>Alveoli</topic><topic>Apoptosis</topic><topic>Cell culture</topic><topic>Computed tomography</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Ethylenediaminetetraacetic acid</topic><topic>Ferroptosis</topic><topic>Gum disease</topic><topic>Health aspects</topic><topic>Histology</topic><topic>Homeostasis</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Lipopolysaccharides</topic><topic>Mitochondria</topic><topic>Osteocytes</topic><topic>Osteoporosis</topic><topic>Pathogenicity</topic><topic>Pathogens</topic><topic>Periodontitis</topic><topic>Proteins</topic><topic>Resveratrol</topic><topic>SOST protein</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Yue</creatorcontrib><creatorcontrib>Huang, Zhijun</creatorcontrib><creatorcontrib>Pan, Shuaifei</creatorcontrib><creatorcontrib>Feng, Yuhui</creatorcontrib><creatorcontrib>He, Haokun</creatorcontrib><creatorcontrib>Cheng, Shuguang</creatorcontrib><creatorcontrib>Wang, Lijing</creatorcontrib><creatorcontrib>Wang, Liping</creatorcontrib><creatorcontrib>Pathak, Janak Lal</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nutrients</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Yue</au><au>Huang, Zhijun</au><au>Pan, Shuaifei</au><au>Feng, Yuhui</au><au>He, Haokun</au><au>Cheng, Shuguang</au><au>Wang, Lijing</au><au>Wang, Liping</au><au>Pathak, Janak Lal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resveratrol Alleviates Diabetic Periodontitis-Induced Alveolar Osteocyte Ferroptosis Possibly via Regulation of SLC7A11/GPX4</atitle><jtitle>Nutrients</jtitle><addtitle>Nutrients</addtitle><date>2023-04-28</date><risdate>2023</risdate><volume>15</volume><issue>9</issue><spage>2115</spage><pages>2115-</pages><issn>2072-6643</issn><eissn>2072-6643</eissn><abstract>The mode and mechanism of diabetic periodontitis-induced alveolar-osteocyte death are still unclear. This study aimed to investigate the occurrence of ferroptosis in alveolar osteocytes during diabetic periodontitis and the therapeutic potential of resveratrol to alleviate osteocyte ferroptosis. Diabetic periodontitis was induced in C57/BL6-male mice and treated with or without resveratrol. Periodontitis pathogenicity was analyzed by micro-CT and histology, and alveolar-osteocyte ferroptosis was analyzed by immunohistochemistry. MLOY4 osteocytes were treated with
-derived lipopolysaccharide (LPS)+advanced glycosylated end products (AGEs) mimicking diabetic periodontitis condition in vitro, with or without resveratrol or ferrostatin-1 (ferroptosis inhibitor). Osteocyte ferroptosis and expression of inflammatory mediators were analyzed. Diabetic periodontitis aggravated periodontitis pathogenicity and inhibited the expression of GPX4 and SLC7A11 in alveolar osteocytes and resveratrol alleviated these effects. LPS+AGEs triggered osteocyte ferroptosis in vitro as indicated by the downregulated GPX4 and SLC7A11, upregulated malondialdehyde, disrupted mitochondrial morphology, and overexpressed pro-inflammatory mediators IL-1β, TNF-α, SOST, RANKL, and IL-6, and ferrostatin-1 or resveratrol treatment reversed these effects. LPS+AGEs upregulated pIKBα and pNF-κB p65 expression in osteocytes, and resveratrol or ferrostatin-1 reversed this effect. In conclusion, diabetic periodontitis triggers alveolar osteocyte ferroptosis possibly via disruption of the SLC7A11/GPX4 axis, and resveratrol has therapeutic potential to correct this biological event.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37432277</pmid><doi>10.3390/nu15092115</doi><orcidid>https://orcid.org/0000-0003-2576-443X</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | Age Alveoli Apoptosis Cell culture Computed tomography Diabetes Diabetes mellitus Ethylenediaminetetraacetic acid Ferroptosis Gum disease Health aspects Histology Homeostasis Immunohistochemistry Inflammation Interleukin 6 Lipid peroxidation Lipids Lipopolysaccharides Mitochondria Osteocytes Osteoporosis Pathogenicity Pathogens Periodontitis Proteins Resveratrol SOST protein Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | Resveratrol Alleviates Diabetic Periodontitis-Induced Alveolar Osteocyte Ferroptosis Possibly via Regulation of SLC7A11/GPX4 |
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