Beneficial effect of magnolol on lupus nephritis in MRL/lpr mice by attenuating the NLRP3 inflammasome and NF‑κB signaling pathway: A mechanistic analysis
Lupus nephritis (LN) is a common complication of systemic lupus erythematosus. The present study aimed to elucidate the protective effect of magnolol (MG) on the progression of LN, via inhibition of key signaling pathways. The results of the present study demonstrated that administration of MG cause...
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| Veröffentlicht in: | Molecular medicine reports 2017-10, Vol.16 (4), p.4817-4822 |
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| description | Lupus nephritis (LN) is a common complication of systemic lupus erythematosus. The present study aimed to elucidate the protective effect of magnolol (MG) on the progression of LN, via inhibition of key signaling pathways. The results of the present study demonstrated that administration of MG caused inhibition of the activation of NACHT, LRR and PYD domains‑containing protein 3 and interleukin‑1β production. Histopathological analysis confirmed that the vehicle‑treated group exhibited characteristic glomerular disease, which was observed to be suppressed following the administration of MG; a marked decrease in glomerular and vascular lesions was observed compared with the vehicle control. This decrease was further demonstrated through analysis of kidney sections. The expression level of cell surface glycoprotein F4/80 was demonstrated to be markedly decreased in the MG‑treated mice compared with the vehicle control group. The MG‑treated mice exhibited a marked decrease in serum and renal tumor necrosis factor‑α expression levels. |
| doi_str_mv | 10.3892/mmr.2017.7154 |
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The present study aimed to elucidate the protective effect of magnolol (MG) on the progression of LN, via inhibition of key signaling pathways. The results of the present study demonstrated that administration of MG caused inhibition of the activation of NACHT, LRR and PYD domains‑containing protein 3 and interleukin‑1β production. Histopathological analysis confirmed that the vehicle‑treated group exhibited characteristic glomerular disease, which was observed to be suppressed following the administration of MG; a marked decrease in glomerular and vascular lesions was observed compared with the vehicle control. This decrease was further demonstrated through analysis of kidney sections. The expression level of cell surface glycoprotein F4/80 was demonstrated to be markedly decreased in the MG‑treated mice compared with the vehicle control group. The MG‑treated mice exhibited a marked decrease in serum and renal tumor necrosis factor‑α expression levels.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.7154</identifier><identifier>PMID: 28791390</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Animals ; Anti-Arrhythmia Agents - pharmacology ; Antibodies, Antinuclear - immunology ; Biopsy ; Biphenyl Compounds - pharmacology ; Cell surface ; Cytokines - metabolism ; Disease Models, Animal ; Female ; Histocytochemistry ; Inflammasomes ; Inflammasomes - metabolism ; Inflammation Mediators - metabolism ; Kidneys ; Kinases ; Lignans - pharmacology ; Lupus ; Lupus nephritis ; Lupus Nephritis - drug therapy ; Lupus Nephritis - immunology ; Lupus Nephritis - metabolism ; Lupus Nephritis - pathology ; Macrophages - immunology ; Macrophages - metabolism ; Macrophages - pathology ; Mice ; Mice, Inbred MRL lpr ; Nephritis ; NF-kappa B - metabolism ; NF-κB protein ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Rodents ; Signal transduction ; Signal Transduction - drug effects ; Studies ; Systemic lupus erythematosus ; Tumor necrosis factor-α</subject><ispartof>Molecular medicine reports, 2017-10, Vol.16 (4), p.4817-4822</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c360t-89285327ba31cbc73c28812fcbb1f3203495bd9762b518e011e9f0d9d0c8d9863</citedby><cites>FETCH-LOGICAL-c360t-89285327ba31cbc73c28812fcbb1f3203495bd9762b518e011e9f0d9d0c8d9863</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28791390$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Feng</creatorcontrib><creatorcontrib>Zhang, Rui-Yun</creatorcontrib><creatorcontrib>Song, Lei</creatorcontrib><title>Beneficial effect of magnolol on lupus nephritis in MRL/lpr mice by attenuating the NLRP3 inflammasome and NF‑κB signaling pathway: A mechanistic analysis</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Lupus nephritis (LN) is a common complication of systemic lupus erythematosus. The present study aimed to elucidate the protective effect of magnolol (MG) on the progression of LN, via inhibition of key signaling pathways. The results of the present study demonstrated that administration of MG caused inhibition of the activation of NACHT, LRR and PYD domains‑containing protein 3 and interleukin‑1β production. Histopathological analysis confirmed that the vehicle‑treated group exhibited characteristic glomerular disease, which was observed to be suppressed following the administration of MG; a marked decrease in glomerular and vascular lesions was observed compared with the vehicle control. This decrease was further demonstrated through analysis of kidney sections. The expression level of cell surface glycoprotein F4/80 was demonstrated to be markedly decreased in the MG‑treated mice compared with the vehicle control group. The MG‑treated mice exhibited a marked decrease in serum and renal tumor necrosis factor‑α expression levels.</description><subject>Animals</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>Antibodies, Antinuclear - immunology</subject><subject>Biopsy</subject><subject>Biphenyl Compounds - pharmacology</subject><subject>Cell surface</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Histocytochemistry</subject><subject>Inflammasomes</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation Mediators - metabolism</subject><subject>Kidneys</subject><subject>Kinases</subject><subject>Lignans - pharmacology</subject><subject>Lupus</subject><subject>Lupus nephritis</subject><subject>Lupus Nephritis - drug therapy</subject><subject>Lupus Nephritis - immunology</subject><subject>Lupus Nephritis - metabolism</subject><subject>Lupus Nephritis - pathology</subject><subject>Macrophages - immunology</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>Mice</subject><subject>Mice, Inbred MRL lpr</subject><subject>Nephritis</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Studies</subject><subject>Systemic lupus erythematosus</subject><subject>Tumor necrosis factor-α</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpd0T1uFDEYgGELgUgIlLTIEk2a2fhnZm3TJREJSEtAEdQjj8fedeSfwfYIbccVOAAXySE4BCfBoywUVP4kP_pk-QXgJUYrygU58z6tCMJsxXDXPgLHmAncUITax4eZCMGOwLOc7xBad6QTT8ER4fWGCnQMfl7ooI1VVjqojdGqwGigl9sQXXQwBujmac4w6GmXbLEZ2gA_3G7O3JSgt0rDYQ9lKTrMstiwhWWn4c3m9hOt0DjpvczRayjDCG-ufn__8ev-Ama7DdItepJl903u38Bz6LXayWBzsapq6fbZ5ufgiZEu6xeH8wR8uXr7-fJds_l4_f7yfNMoukalqf_AO0rYIClWg2JUEc4xMWoYsKEE0VZ0wyjYmgwd5hphrIVBoxiR4qPga3oCTh_2Til-nXUuvbdZaedk0HHOPRaEdYIjIip9_R-9i3Oq710UR4jxrm2rah6USjHnpE0_Jetl2vcY9Uu3vnbrl2790q36V4et8-D1-E__DUX_AJFOlb0</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Huang, Feng</creator><creator>Zhang, Rui-Yun</creator><creator>Song, Lei</creator><general>Spandidos Publications UK Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20171001</creationdate><title>Beneficial effect of magnolol on lupus nephritis in MRL/lpr mice by attenuating the NLRP3 inflammasome and NF‑κB signaling pathway: A mechanistic analysis</title><author>Huang, Feng ; Zhang, Rui-Yun ; Song, Lei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c360t-89285327ba31cbc73c28812fcbb1f3203495bd9762b518e011e9f0d9d0c8d9863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>Antibodies, Antinuclear - immunology</topic><topic>Biopsy</topic><topic>Biphenyl Compounds - pharmacology</topic><topic>Cell surface</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Histocytochemistry</topic><topic>Inflammasomes</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation Mediators - metabolism</topic><topic>Kidneys</topic><topic>Kinases</topic><topic>Lignans - pharmacology</topic><topic>Lupus</topic><topic>Lupus nephritis</topic><topic>Lupus Nephritis - drug therapy</topic><topic>Lupus Nephritis - immunology</topic><topic>Lupus Nephritis - metabolism</topic><topic>Lupus Nephritis - pathology</topic><topic>Macrophages - immunology</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - pathology</topic><topic>Mice</topic><topic>Mice, Inbred MRL lpr</topic><topic>Nephritis</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Studies</topic><topic>Systemic lupus erythematosus</topic><topic>Tumor necrosis factor-α</topic><toplevel>online_resources</toplevel><creatorcontrib>Huang, Feng</creatorcontrib><creatorcontrib>Zhang, Rui-Yun</creatorcontrib><creatorcontrib>Song, Lei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>British Nursing Database</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>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science 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>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Feng</au><au>Zhang, Rui-Yun</au><au>Song, Lei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Beneficial effect of magnolol on lupus nephritis in MRL/lpr mice by attenuating the NLRP3 inflammasome and NF‑κB signaling pathway: A mechanistic analysis</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>16</volume><issue>4</issue><spage>4817</spage><epage>4822</epage><pages>4817-4822</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Lupus nephritis (LN) is a common complication of systemic lupus erythematosus. The present study aimed to elucidate the protective effect of magnolol (MG) on the progression of LN, via inhibition of key signaling pathways. The results of the present study demonstrated that administration of MG caused inhibition of the activation of NACHT, LRR and PYD domains‑containing protein 3 and interleukin‑1β production. Histopathological analysis confirmed that the vehicle‑treated group exhibited characteristic glomerular disease, which was observed to be suppressed following the administration of MG; a marked decrease in glomerular and vascular lesions was observed compared with the vehicle control. This decrease was further demonstrated through analysis of kidney sections. The expression level of cell surface glycoprotein F4/80 was demonstrated to be markedly decreased in the MG‑treated mice compared with the vehicle control group. The MG‑treated mice exhibited a marked decrease in serum and renal tumor necrosis factor‑α expression levels.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>28791390</pmid><doi>10.3892/mmr.2017.7154</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Anti-Arrhythmia Agents - pharmacology Antibodies, Antinuclear - immunology Biopsy Biphenyl Compounds - pharmacology Cell surface Cytokines - metabolism Disease Models, Animal Female Histocytochemistry Inflammasomes Inflammasomes - metabolism Inflammation Mediators - metabolism Kidneys Kinases Lignans - pharmacology Lupus Lupus nephritis Lupus Nephritis - drug therapy Lupus Nephritis - immunology Lupus Nephritis - metabolism Lupus Nephritis - pathology Macrophages - immunology Macrophages - metabolism Macrophages - pathology Mice Mice, Inbred MRL lpr Nephritis NF-kappa B - metabolism NF-κB protein NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Rodents Signal transduction Signal Transduction - drug effects Studies Systemic lupus erythematosus Tumor necrosis factor-α |
| title | Beneficial effect of magnolol on lupus nephritis in MRL/lpr mice by attenuating the NLRP3 inflammasome and NF‑κB signaling pathway: A mechanistic analysis |
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