Protection against Oxidative Stress by Coenzyme Q10 in a Porcine Retinal Degeneration Model
Oxidative stress plays an important role in neurodegenerative diseases, including glaucoma. Therefore, we analyzed if the antioxidant coenzyme Q10 (CoQ10), which is also commercially available, can prevent retinal degeneration induced by hydrogen peroxide (H O ) in a porcine organ culture model. Ret...
Gespeichert in:
| Veröffentlicht in: | Journal of personalized medicine 2024-04, Vol.14 (4), p.437 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 4 |
| container_start_page | 437 |
| container_title | Journal of personalized medicine |
| container_volume | 14 |
| creator | Deppe, Leonie Mueller-Buehl, Ana M Tsai, Teresa Erb, Carl Dick, H Burkhard Joachim, Stephanie C |
| description | Oxidative stress plays an important role in neurodegenerative diseases, including glaucoma. Therefore, we analyzed if the antioxidant coenzyme Q10 (CoQ10), which is also commercially available, can prevent retinal degeneration induced by hydrogen peroxide (H
O
) in a porcine organ culture model. Retinal explants were cultivated for eight days, and H
O
(500 µM, 3 h) induced the oxidative damage. CoQ10 therapy was applied (700 µM, 48 h). Retinal ganglion cells (RGCs) and microglia were examined immunohistologically in all groups (control, H
O
, H
O
+ CoQ10). Cellular, oxidative, and inflammatory genes were quantified via RT-qPCR. Strong RGC loss was observed with H
O
(
≤ 0.001). CoQ10 elicited RGC protection compared to the damaged group at a histological (
≤ 0.001) and mRNA level. We detected more microglia cells with H
O
, but CoQ10 reduced this effect (
= 0.004). Cellular protection genes (
) against oxidative stress were stimulated by CoQ10 (
≤ 0.001). Furthermore, mitochondrial oxidative stress (
) increased through H
O
(
= 0.038), and CoQ10 reduced it to control level. Our novel results indicate neuroprotection via CoQ10 in porcine retina organ cultures. In particular, CoQ10 appears to protect RGCs by potentially inhibiting apoptosis-related pathways, activating intracellular protection and reducing mitochondrial stress. |
| doi_str_mv | 10.3390/jpm14040437 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_3047950464</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A793553003</galeid><sourcerecordid>A793553003</sourcerecordid><originalsourceid>FETCH-LOGICAL-c379t-3ef165ac95566f78df678f8436f1fa0e064d124f934417b932033899527e14193</originalsourceid><addsrcrecordid>eNptkcuLFDEQxoMo7jLuybsEvAgya5LKo3Ncxies7Po6eWgy3ZUhQ3cyJhlx_OvNuquuYtWhiuJXHx98hDzk7BTAsmfb3cwlaw3mDjkWzKillELfvbUfkZNStqxVp4TQ7D45gk4bYFodk8-XOVUcakiRuo0LsVR68S2MroavSD_UjKXQ9YGuEsbvhxnpO85oaCy9THkIEel7rCG6iT7HDUbM7qfU2zTi9IDc824qeHIzF-TTyxcfV6-X5xev3qzOzpcDGFuXgJ5r5QarlNbedKPXpvOdBO25dwyZliMX0luQkpu1BcEAOmuVMMglt7AgT651dzl92WOp_RzKgNPkIqZ96YFJYxWTWjb08T_oNu1zs98oLrTthGXiD7VxE_Yh-lSzG65E-zNjQSlgzcKCnP6Haj3iHIYU0Yd2_-vh6fXDkFMpGX2_y2F2-dBz1l-l2d9Ks9GPbqzu1zOOv9lf2cEPfZ6Vmw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3126982902</pqid></control><display><type>article</type><title>Protection against Oxidative Stress by Coenzyme Q10 in a Porcine Retinal Degeneration Model</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central Open Access</source><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>PubMed Central</source><creator>Deppe, Leonie ; Mueller-Buehl, Ana M ; Tsai, Teresa ; Erb, Carl ; Dick, H Burkhard ; Joachim, Stephanie C</creator><creatorcontrib>Deppe, Leonie ; Mueller-Buehl, Ana M ; Tsai, Teresa ; Erb, Carl ; Dick, H Burkhard ; Joachim, Stephanie C</creatorcontrib><description>Oxidative stress plays an important role in neurodegenerative diseases, including glaucoma. Therefore, we analyzed if the antioxidant coenzyme Q10 (CoQ10), which is also commercially available, can prevent retinal degeneration induced by hydrogen peroxide (H
O
) in a porcine organ culture model. Retinal explants were cultivated for eight days, and H
O
(500 µM, 3 h) induced the oxidative damage. CoQ10 therapy was applied (700 µM, 48 h). Retinal ganglion cells (RGCs) and microglia were examined immunohistologically in all groups (control, H
O
, H
O
+ CoQ10). Cellular, oxidative, and inflammatory genes were quantified via RT-qPCR. Strong RGC loss was observed with H
O
(
≤ 0.001). CoQ10 elicited RGC protection compared to the damaged group at a histological (
≤ 0.001) and mRNA level. We detected more microglia cells with H
O
, but CoQ10 reduced this effect (
= 0.004). Cellular protection genes (
) against oxidative stress were stimulated by CoQ10 (
≤ 0.001). Furthermore, mitochondrial oxidative stress (
) increased through H
O
(
= 0.038), and CoQ10 reduced it to control level. Our novel results indicate neuroprotection via CoQ10 in porcine retina organ cultures. In particular, CoQ10 appears to protect RGCs by potentially inhibiting apoptosis-related pathways, activating intracellular protection and reducing mitochondrial stress.</description><identifier>ISSN: 2075-4426</identifier><identifier>EISSN: 2075-4426</identifier><identifier>DOI: 10.3390/jpm14040437</identifier><identifier>PMID: 38673065</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Apoptosis ; Cell culture ; Coenzyme Q10 ; Diabetic retinopathy ; Enzymes ; Explants ; Glaucoma ; Hydrogen peroxide ; Inflammation ; Macular degeneration ; Medical research ; Microglia ; mRNA ; Neurodegeneration ; Neurodegenerative diseases ; Neuroprotection ; Organ culture ; Oxidative stress ; Pathology ; Physiological aspects ; Retina ; Retinal degeneration ; Retinal ganglion cells ; Scientific equipment and supplies industry ; Signal transduction</subject><ispartof>Journal of personalized medicine, 2024-04, Vol.14 (4), p.437</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c379t-3ef165ac95566f78df678f8436f1fa0e064d124f934417b932033899527e14193</cites><orcidid>0000-0001-6041-1264 ; 0000-0001-7056-0829</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38673065$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deppe, Leonie</creatorcontrib><creatorcontrib>Mueller-Buehl, Ana M</creatorcontrib><creatorcontrib>Tsai, Teresa</creatorcontrib><creatorcontrib>Erb, Carl</creatorcontrib><creatorcontrib>Dick, H Burkhard</creatorcontrib><creatorcontrib>Joachim, Stephanie C</creatorcontrib><title>Protection against Oxidative Stress by Coenzyme Q10 in a Porcine Retinal Degeneration Model</title><title>Journal of personalized medicine</title><addtitle>J Pers Med</addtitle><description>Oxidative stress plays an important role in neurodegenerative diseases, including glaucoma. Therefore, we analyzed if the antioxidant coenzyme Q10 (CoQ10), which is also commercially available, can prevent retinal degeneration induced by hydrogen peroxide (H
O
) in a porcine organ culture model. Retinal explants were cultivated for eight days, and H
O
(500 µM, 3 h) induced the oxidative damage. CoQ10 therapy was applied (700 µM, 48 h). Retinal ganglion cells (RGCs) and microglia were examined immunohistologically in all groups (control, H
O
, H
O
+ CoQ10). Cellular, oxidative, and inflammatory genes were quantified via RT-qPCR. Strong RGC loss was observed with H
O
(
≤ 0.001). CoQ10 elicited RGC protection compared to the damaged group at a histological (
≤ 0.001) and mRNA level. We detected more microglia cells with H
O
, but CoQ10 reduced this effect (
= 0.004). Cellular protection genes (
) against oxidative stress were stimulated by CoQ10 (
≤ 0.001). Furthermore, mitochondrial oxidative stress (
) increased through H
O
(
= 0.038), and CoQ10 reduced it to control level. Our novel results indicate neuroprotection via CoQ10 in porcine retina organ cultures. In particular, CoQ10 appears to protect RGCs by potentially inhibiting apoptosis-related pathways, activating intracellular protection and reducing mitochondrial stress.</description><subject>Apoptosis</subject><subject>Cell culture</subject><subject>Coenzyme Q10</subject><subject>Diabetic retinopathy</subject><subject>Enzymes</subject><subject>Explants</subject><subject>Glaucoma</subject><subject>Hydrogen peroxide</subject><subject>Inflammation</subject><subject>Macular degeneration</subject><subject>Medical research</subject><subject>Microglia</subject><subject>mRNA</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neuroprotection</subject><subject>Organ culture</subject><subject>Oxidative stress</subject><subject>Pathology</subject><subject>Physiological aspects</subject><subject>Retina</subject><subject>Retinal degeneration</subject><subject>Retinal ganglion cells</subject><subject>Scientific equipment and supplies industry</subject><subject>Signal transduction</subject><issn>2075-4426</issn><issn>2075-4426</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkcuLFDEQxoMo7jLuybsEvAgya5LKo3Ncxies7Po6eWgy3ZUhQ3cyJhlx_OvNuquuYtWhiuJXHx98hDzk7BTAsmfb3cwlaw3mDjkWzKillELfvbUfkZNStqxVp4TQ7D45gk4bYFodk8-XOVUcakiRuo0LsVR68S2MroavSD_UjKXQ9YGuEsbvhxnpO85oaCy9THkIEel7rCG6iT7HDUbM7qfU2zTi9IDc824qeHIzF-TTyxcfV6-X5xev3qzOzpcDGFuXgJ5r5QarlNbedKPXpvOdBO25dwyZliMX0luQkpu1BcEAOmuVMMglt7AgT651dzl92WOp_RzKgNPkIqZ96YFJYxWTWjb08T_oNu1zs98oLrTthGXiD7VxE_Yh-lSzG65E-zNjQSlgzcKCnP6Haj3iHIYU0Yd2_-vh6fXDkFMpGX2_y2F2-dBz1l-l2d9Ks9GPbqzu1zOOv9lf2cEPfZ6Vmw</recordid><startdate>20240401</startdate><enddate>20240401</enddate><creator>Deppe, Leonie</creator><creator>Mueller-Buehl, Ana M</creator><creator>Tsai, Teresa</creator><creator>Erb, Carl</creator><creator>Dick, H Burkhard</creator><creator>Joachim, Stephanie C</creator><general>MDPI AG</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-6041-1264</orcidid><orcidid>https://orcid.org/0000-0001-7056-0829</orcidid></search><sort><creationdate>20240401</creationdate><title>Protection against Oxidative Stress by Coenzyme Q10 in a Porcine Retinal Degeneration Model</title><author>Deppe, Leonie ; Mueller-Buehl, Ana M ; Tsai, Teresa ; Erb, Carl ; Dick, H Burkhard ; Joachim, Stephanie C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c379t-3ef165ac95566f78df678f8436f1fa0e064d124f934417b932033899527e14193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Apoptosis</topic><topic>Cell culture</topic><topic>Coenzyme Q10</topic><topic>Diabetic retinopathy</topic><topic>Enzymes</topic><topic>Explants</topic><topic>Glaucoma</topic><topic>Hydrogen peroxide</topic><topic>Inflammation</topic><topic>Macular degeneration</topic><topic>Medical research</topic><topic>Microglia</topic><topic>mRNA</topic><topic>Neurodegeneration</topic><topic>Neurodegenerative diseases</topic><topic>Neuroprotection</topic><topic>Organ culture</topic><topic>Oxidative stress</topic><topic>Pathology</topic><topic>Physiological aspects</topic><topic>Retina</topic><topic>Retinal degeneration</topic><topic>Retinal ganglion cells</topic><topic>Scientific equipment and supplies industry</topic><topic>Signal transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Deppe, Leonie</creatorcontrib><creatorcontrib>Mueller-Buehl, Ana M</creatorcontrib><creatorcontrib>Tsai, Teresa</creatorcontrib><creatorcontrib>Erb, Carl</creatorcontrib><creatorcontrib>Dick, H Burkhard</creatorcontrib><creatorcontrib>Joachim, Stephanie C</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science 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><jtitle>Journal of personalized medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deppe, Leonie</au><au>Mueller-Buehl, Ana M</au><au>Tsai, Teresa</au><au>Erb, Carl</au><au>Dick, H Burkhard</au><au>Joachim, Stephanie C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protection against Oxidative Stress by Coenzyme Q10 in a Porcine Retinal Degeneration Model</atitle><jtitle>Journal of personalized medicine</jtitle><addtitle>J Pers Med</addtitle><date>2024-04-01</date><risdate>2024</risdate><volume>14</volume><issue>4</issue><spage>437</spage><pages>437-</pages><issn>2075-4426</issn><eissn>2075-4426</eissn><abstract>Oxidative stress plays an important role in neurodegenerative diseases, including glaucoma. Therefore, we analyzed if the antioxidant coenzyme Q10 (CoQ10), which is also commercially available, can prevent retinal degeneration induced by hydrogen peroxide (H
O
) in a porcine organ culture model. Retinal explants were cultivated for eight days, and H
O
(500 µM, 3 h) induced the oxidative damage. CoQ10 therapy was applied (700 µM, 48 h). Retinal ganglion cells (RGCs) and microglia were examined immunohistologically in all groups (control, H
O
, H
O
+ CoQ10). Cellular, oxidative, and inflammatory genes were quantified via RT-qPCR. Strong RGC loss was observed with H
O
(
≤ 0.001). CoQ10 elicited RGC protection compared to the damaged group at a histological (
≤ 0.001) and mRNA level. We detected more microglia cells with H
O
, but CoQ10 reduced this effect (
= 0.004). Cellular protection genes (
) against oxidative stress were stimulated by CoQ10 (
≤ 0.001). Furthermore, mitochondrial oxidative stress (
) increased through H
O
(
= 0.038), and CoQ10 reduced it to control level. Our novel results indicate neuroprotection via CoQ10 in porcine retina organ cultures. In particular, CoQ10 appears to protect RGCs by potentially inhibiting apoptosis-related pathways, activating intracellular protection and reducing mitochondrial stress.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>38673065</pmid><doi>10.3390/jpm14040437</doi><orcidid>https://orcid.org/0000-0001-6041-1264</orcidid><orcidid>https://orcid.org/0000-0001-7056-0829</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2075-4426 |
| ispartof | Journal of personalized medicine, 2024-04, Vol.14 (4), p.437 |
| issn | 2075-4426 2075-4426 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_3047950464 |
| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; MDPI - Multidisciplinary Digital Publishing Institute; PubMed Central |
| subjects | Apoptosis Cell culture Coenzyme Q10 Diabetic retinopathy Enzymes Explants Glaucoma Hydrogen peroxide Inflammation Macular degeneration Medical research Microglia mRNA Neurodegeneration Neurodegenerative diseases Neuroprotection Organ culture Oxidative stress Pathology Physiological aspects Retina Retinal degeneration Retinal ganglion cells Scientific equipment and supplies industry Signal transduction |
| title | Protection against Oxidative Stress by Coenzyme Q10 in a Porcine Retinal Degeneration Model |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-08T06%3A45%3A45IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Protection%20against%20Oxidative%20Stress%20by%20Coenzyme%20Q10%20in%20a%20Porcine%20Retinal%20Degeneration%20Model&rft.jtitle=Journal%20of%20personalized%20medicine&rft.au=Deppe,%20Leonie&rft.date=2024-04-01&rft.volume=14&rft.issue=4&rft.spage=437&rft.pages=437-&rft.issn=2075-4426&rft.eissn=2075-4426&rft_id=info:doi/10.3390/jpm14040437&rft_dat=%3Cgale_proqu%3EA793553003%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3126982902&rft_id=info:pmid/38673065&rft_galeid=A793553003&rfr_iscdi=true |