Ursolic acid alleviates inflammation and against diabetes‑induced nephropathy through TLR4‑mediated inflammatory pathway
Ursolic acid (UA) is a triterpenoid isolated from Chinese herbal medicine. It is extensively distributed in the plant kingdom in at least 63 Chinese herbal medicines of 26 families. UA has multiple bioactivities, including anti‑viral hepatitis, antitumor, anti‑oxidation, anti‑bacterium and anti‑infl...
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| Veröffentlicht in: | Molecular medicine reports 2018-11, Vol.18 (5), p.4675-4681 |
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| creator | Li, Jian Li, Nan Yan, Shuangtong Liu, Minyan Sun, Banruo Lu, Yanhui Shao, Yinghong |
| description | Ursolic acid (UA) is a triterpenoid isolated from Chinese herbal medicine. It is extensively distributed in the plant kingdom in at least 63 Chinese herbal medicines of 26 families. UA has multiple bioactivities, including anti‑viral hepatitis, antitumor, anti‑oxidation, anti‑bacterium and anti‑inflammation. The aim of this in vitro study was to examine the effects of UA on diabetes‑induced nephropathy and its possible mechanism. In mice with diabetes‑induced nephropathy, UA increased the body weight, reduced kidney/body weight index, protected kidney cells, alleviated inflammation [tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 levels] and kidney cell damage. It was also indicated that UA suppressed Toll‑like receptor 4 (TLR4), myeloid differentiation factor 88 and nuclear factor‑κB protein expression in mice with diabetes‑induced nephropathy. The inhibition of TLR4 increased the anti‑inflammation of UA on inflammation in rat with diabetes‑induced nephropathy through the TLR4 signaling pathway. In conclusion, UA alleviates inflammation and inhibits diabetes‑induced nephropathy through a TLR4‑mediated inflammatory pathway. The present findings indicated that UA may be a possible therapeutic agent against diabetic nephropathy. |
| doi_str_mv | 10.3892/mmr.2018.9429 |
| format | Article |
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It is extensively distributed in the plant kingdom in at least 63 Chinese herbal medicines of 26 families. UA has multiple bioactivities, including anti‑viral hepatitis, antitumor, anti‑oxidation, anti‑bacterium and anti‑inflammation. The aim of this in vitro study was to examine the effects of UA on diabetes‑induced nephropathy and its possible mechanism. In mice with diabetes‑induced nephropathy, UA increased the body weight, reduced kidney/body weight index, protected kidney cells, alleviated inflammation [tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 levels] and kidney cell damage. It was also indicated that UA suppressed Toll‑like receptor 4 (TLR4), myeloid differentiation factor 88 and nuclear factor‑κB protein expression in mice with diabetes‑induced nephropathy. The inhibition of TLR4 increased the anti‑inflammation of UA on inflammation in rat with diabetes‑induced nephropathy through the TLR4 signaling pathway. In conclusion, UA alleviates inflammation and inhibits diabetes‑induced nephropathy through a TLR4‑mediated inflammatory pathway. The present findings indicated that UA may be a possible therapeutic agent against diabetic nephropathy.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2018.9429</identifier><identifier>PMID: 30221655</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Animals ; Antiviral agents ; Apoptosis ; Body weight ; Cellular signal transduction ; Diabetes ; Diabetes mellitus ; Diabetic nephropathies ; Diabetic Nephropathies - complications ; Diabetic Nephropathies - drug therapy ; Diabetic Nephropathies - genetics ; Diabetic Nephropathies - pathology ; Diabetic nephropathy ; Disease Models, Animal ; Drugs, Chinese Herbal - administration & dosage ; Drugs, Chinese Herbal - chemistry ; Gene Expression Regulation - drug effects ; Genetic aspects ; Health aspects ; Hepatitis ; Herbal medicine ; Humans ; Hyperglycemia ; Inflammation ; Inflammation - complications ; Inflammation - drug therapy ; Inflammation - genetics ; Inflammation - pathology ; Interleukin 18 ; Interleukin 6 ; Kidney - drug effects ; Kidney - pathology ; Kidneys ; Laboratory animals ; Ligands ; Medicinal plants ; Membranes ; Metabolism ; Mice ; MyD88 protein ; Myeloid Differentiation Factor 88 - genetics ; Nephropathy ; NF-kappa B - genetics ; Oxidation ; Oxidative Stress - drug effects ; Physiology ; Prevention ; Proteins ; Rats ; Rodents ; Signal transduction ; Signal Transduction - genetics ; Statistical analysis ; Terpenoids ; TLR4 protein ; Toll-Like Receptor 4 - genetics ; Toll-like receptors ; Transcription factors ; Triterpenes - administration & dosage ; Triterpenes - chemistry ; Tumor Necrosis Factor-alpha - genetics ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Ursolic Acid</subject><ispartof>Molecular medicine reports, 2018-11, Vol.18 (5), p.4675-4681</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-d6c7918a3cebb0c1254c9742b50d00fc996e9eaf58a1d1da7bb04278c96f04a53</citedby><cites>FETCH-LOGICAL-c427t-d6c7918a3cebb0c1254c9742b50d00fc996e9eaf58a1d1da7bb04278c96f04a53</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/30221655$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Jian</creatorcontrib><creatorcontrib>Li, Nan</creatorcontrib><creatorcontrib>Yan, Shuangtong</creatorcontrib><creatorcontrib>Liu, Minyan</creatorcontrib><creatorcontrib>Sun, Banruo</creatorcontrib><creatorcontrib>Lu, Yanhui</creatorcontrib><creatorcontrib>Shao, Yinghong</creatorcontrib><title>Ursolic acid alleviates inflammation and against diabetes‑induced nephropathy through TLR4‑mediated inflammatory pathway</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Ursolic acid (UA) is a triterpenoid isolated from Chinese herbal medicine. It is extensively distributed in the plant kingdom in at least 63 Chinese herbal medicines of 26 families. UA has multiple bioactivities, including anti‑viral hepatitis, antitumor, anti‑oxidation, anti‑bacterium and anti‑inflammation. The aim of this in vitro study was to examine the effects of UA on diabetes‑induced nephropathy and its possible mechanism. In mice with diabetes‑induced nephropathy, UA increased the body weight, reduced kidney/body weight index, protected kidney cells, alleviated inflammation [tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 levels] and kidney cell damage. It was also indicated that UA suppressed Toll‑like receptor 4 (TLR4), myeloid differentiation factor 88 and nuclear factor‑κB protein expression in mice with diabetes‑induced nephropathy. The inhibition of TLR4 increased the anti‑inflammation of UA on inflammation in rat with diabetes‑induced nephropathy through the TLR4 signaling pathway. In conclusion, UA alleviates inflammation and inhibits diabetes‑induced nephropathy through a TLR4‑mediated inflammatory pathway. The present findings indicated that UA may be a possible therapeutic agent against diabetic nephropathy.</description><subject>Animals</subject><subject>Antiviral agents</subject><subject>Apoptosis</subject><subject>Body weight</subject><subject>Cellular signal transduction</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetic nephropathies</subject><subject>Diabetic Nephropathies - complications</subject><subject>Diabetic Nephropathies - drug therapy</subject><subject>Diabetic Nephropathies - genetics</subject><subject>Diabetic Nephropathies - pathology</subject><subject>Diabetic nephropathy</subject><subject>Disease Models, Animal</subject><subject>Drugs, Chinese Herbal - administration & dosage</subject><subject>Drugs, Chinese Herbal - chemistry</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Hepatitis</subject><subject>Herbal medicine</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Inflammation</subject><subject>Inflammation - complications</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - genetics</subject><subject>Inflammation - pathology</subject><subject>Interleukin 18</subject><subject>Interleukin 6</subject><subject>Kidney - drug effects</subject><subject>Kidney - pathology</subject><subject>Kidneys</subject><subject>Laboratory animals</subject><subject>Ligands</subject><subject>Medicinal plants</subject><subject>Membranes</subject><subject>Metabolism</subject><subject>Mice</subject><subject>MyD88 protein</subject><subject>Myeloid Differentiation Factor 88 - genetics</subject><subject>Nephropathy</subject><subject>NF-kappa B - genetics</subject><subject>Oxidation</subject><subject>Oxidative Stress - drug effects</subject><subject>Physiology</subject><subject>Prevention</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Signal Transduction - genetics</subject><subject>Statistical analysis</subject><subject>Terpenoids</subject><subject>TLR4 protein</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-like receptors</subject><subject>Transcription factors</subject><subject>Triterpenes - administration & dosage</subject><subject>Triterpenes - chemistry</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Ursolic Acid</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</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>eNptkc1q3DAUhUVpaX7aZbZF0LUnkmzJ0jKE_MFAICRrcS3JMwq2NZHshIEs-gp9xTxJZDJpCBQtdJG-c-6VDkJHlCxKqdhx38cFI1QuVMXUF7RPa0WLkpDq665mStV76CCle0IEZ1x9R3slYYwKzvfR811MofMGg_EWQ9e5Rw-jS9gPbQd9D6MPA4Yh363AD2nE1kPjMvHy568f7GScxYPbrGPYwLje4jFX02qNb5c3VUZ6Z2c_--EX4hbP6BNsf6BvLXTJ_dzth-ju_Oz29LJYXl9cnZ4sC1OxeiysMPkhEkrjmoYYynhlVF2xhhNLSGuUEk45aLkEaqmFOlNZKI0SLamAl4fo95vvJoaHyaVR34cpDrmlZpSKWlJJxQe1gs7pPG8YI5jeJ6NPOFdCikrO1OI_VF7W9d6EwbU-n38SFG8CE0NK0bV6E30Pcasp0XOEOkeo5wj1HGHmf-2GnZr8e__o98zKV8DDmpU</recordid><startdate>20181101</startdate><enddate>20181101</enddate><creator>Li, Jian</creator><creator>Li, Nan</creator><creator>Yan, Shuangtong</creator><creator>Liu, Minyan</creator><creator>Sun, Banruo</creator><creator>Lu, Yanhui</creator><creator>Shao, Yinghong</creator><general>Spandidos Publications</general><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></search><sort><creationdate>20181101</creationdate><title>Ursolic acid alleviates inflammation and against diabetes‑induced nephropathy through TLR4‑mediated inflammatory pathway</title><author>Li, Jian ; Li, Nan ; Yan, Shuangtong ; Liu, Minyan ; Sun, Banruo ; Lu, Yanhui ; Shao, Yinghong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-d6c7918a3cebb0c1254c9742b50d00fc996e9eaf58a1d1da7bb04278c96f04a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Antiviral agents</topic><topic>Apoptosis</topic><topic>Body weight</topic><topic>Cellular signal transduction</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetic nephropathies</topic><topic>Diabetic Nephropathies - complications</topic><topic>Diabetic Nephropathies - drug therapy</topic><topic>Diabetic Nephropathies - genetics</topic><topic>Diabetic Nephropathies - pathology</topic><topic>Diabetic nephropathy</topic><topic>Disease Models, Animal</topic><topic>Drugs, Chinese Herbal - administration & dosage</topic><topic>Drugs, Chinese Herbal - chemistry</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Hepatitis</topic><topic>Herbal medicine</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Inflammation</topic><topic>Inflammation - complications</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - genetics</topic><topic>Inflammation - pathology</topic><topic>Interleukin 18</topic><topic>Interleukin 6</topic><topic>Kidney - drug effects</topic><topic>Kidney - pathology</topic><topic>Kidneys</topic><topic>Laboratory animals</topic><topic>Ligands</topic><topic>Medicinal plants</topic><topic>Membranes</topic><topic>Metabolism</topic><topic>Mice</topic><topic>MyD88 protein</topic><topic>Myeloid Differentiation Factor 88 - genetics</topic><topic>Nephropathy</topic><topic>NF-kappa B - genetics</topic><topic>Oxidation</topic><topic>Oxidative Stress - drug effects</topic><topic>Physiology</topic><topic>Prevention</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Signal Transduction - genetics</topic><topic>Statistical analysis</topic><topic>Terpenoids</topic><topic>TLR4 protein</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-like receptors</topic><topic>Transcription factors</topic><topic>Triterpenes - administration & dosage</topic><topic>Triterpenes - chemistry</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Ursolic Acid</topic><toplevel>online_resources</toplevel><creatorcontrib>Li, Jian</creatorcontrib><creatorcontrib>Li, Nan</creatorcontrib><creatorcontrib>Yan, Shuangtong</creatorcontrib><creatorcontrib>Liu, Minyan</creatorcontrib><creatorcontrib>Sun, Banruo</creatorcontrib><creatorcontrib>Lu, Yanhui</creatorcontrib><creatorcontrib>Shao, Yinghong</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><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Jian</au><au>Li, Nan</au><au>Yan, Shuangtong</au><au>Liu, Minyan</au><au>Sun, Banruo</au><au>Lu, Yanhui</au><au>Shao, Yinghong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ursolic acid alleviates inflammation and against diabetes‑induced nephropathy through TLR4‑mediated inflammatory pathway</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-11-01</date><risdate>2018</risdate><volume>18</volume><issue>5</issue><spage>4675</spage><epage>4681</epage><pages>4675-4681</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Ursolic acid (UA) is a triterpenoid isolated from Chinese herbal medicine. It is extensively distributed in the plant kingdom in at least 63 Chinese herbal medicines of 26 families. UA has multiple bioactivities, including anti‑viral hepatitis, antitumor, anti‑oxidation, anti‑bacterium and anti‑inflammation. The aim of this in vitro study was to examine the effects of UA on diabetes‑induced nephropathy and its possible mechanism. In mice with diabetes‑induced nephropathy, UA increased the body weight, reduced kidney/body weight index, protected kidney cells, alleviated inflammation [tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 levels] and kidney cell damage. It was also indicated that UA suppressed Toll‑like receptor 4 (TLR4), myeloid differentiation factor 88 and nuclear factor‑κB protein expression in mice with diabetes‑induced nephropathy. The inhibition of TLR4 increased the anti‑inflammation of UA on inflammation in rat with diabetes‑induced nephropathy through the TLR4 signaling pathway. In conclusion, UA alleviates inflammation and inhibits diabetes‑induced nephropathy through a TLR4‑mediated inflammatory pathway. The present findings indicated that UA may be a possible therapeutic agent against diabetic nephropathy.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30221655</pmid><doi>10.3892/mmr.2018.9429</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular medicine reports, 2018-11, Vol.18 (5), p.4675-4681 |
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| language | eng |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Antiviral agents Apoptosis Body weight Cellular signal transduction Diabetes Diabetes mellitus Diabetic nephropathies Diabetic Nephropathies - complications Diabetic Nephropathies - drug therapy Diabetic Nephropathies - genetics Diabetic Nephropathies - pathology Diabetic nephropathy Disease Models, Animal Drugs, Chinese Herbal - administration & dosage Drugs, Chinese Herbal - chemistry Gene Expression Regulation - drug effects Genetic aspects Health aspects Hepatitis Herbal medicine Humans Hyperglycemia Inflammation Inflammation - complications Inflammation - drug therapy Inflammation - genetics Inflammation - pathology Interleukin 18 Interleukin 6 Kidney - drug effects Kidney - pathology Kidneys Laboratory animals Ligands Medicinal plants Membranes Metabolism Mice MyD88 protein Myeloid Differentiation Factor 88 - genetics Nephropathy NF-kappa B - genetics Oxidation Oxidative Stress - drug effects Physiology Prevention Proteins Rats Rodents Signal transduction Signal Transduction - genetics Statistical analysis Terpenoids TLR4 protein Toll-Like Receptor 4 - genetics Toll-like receptors Transcription factors Triterpenes - administration & dosage Triterpenes - chemistry Tumor Necrosis Factor-alpha - genetics Tumor necrosis factor-TNF Tumor necrosis factor-α Ursolic Acid |
| title | Ursolic acid alleviates inflammation and against diabetes‑induced nephropathy through TLR4‑mediated inflammatory pathway |
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