Effect of Rosmarinic Acid on Experimental Diabetic Nephropathy
: Connective tissue growth factor (CTGF) plays a pathogenic role in diabetic nephropathy (DN). Rosmarinic acid (RA) is a naturally occurring phenolic acid. This study was conducted to investigate the efficacy of RA on DN and to elucidate the potential mechanism. High glucose (HG)‐stimulated culture...
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| Veröffentlicht in: | Basic & clinical pharmacology & toxicology 2012-04, Vol.110 (4), p.390-395 |
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| description | : Connective tissue growth factor (CTGF) plays a pathogenic role in diabetic nephropathy (DN). Rosmarinic acid (RA) is a naturally occurring phenolic acid. This study was conducted to investigate the efficacy of RA on DN and to elucidate the potential mechanism. High glucose (HG)‐stimulated cultured human renal proximal tubular epithelial cells (HK‐2) analysed CTGF expression by western blotting, and it was investigated whether extracellular signal‐regulated kinase (ERK) signalling pathway was involved. Using streptozotocin (STZ)‐induced rat animal models, diabetic rats were randomized to receive intragastric (i.g.) doses of RA. Renal tissue, blood and urine samples were collected to determine biochemical index and analyse protein expression. In vitro study, RA reduced CTGF excretion in HG‐induced HK‐2 cells through the ERK signalling pathway. In an in vivo study, I.g. of RA 7.5 or 15 mg/kg significantly ameliorated renal function and increased body‐weight. Meanwhile, RA reduced renal CTGF expression by immunohistochemical staining and reduced serum levels of CTGF. Besides, there were no significant differences in glycaemia levels between the RA groups compared with the STZ‐treated group. Furthermore, RA ameliorated renal pathology. These results suggest that RA exerts an early renal protective role to DN. Inhibition of CTGF may be a potential target in DN therapy, which highlights the possibility of using RA in the treatment of DN. |
| doi_str_mv | 10.1111/j.1742-7843.2011.00828.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1008841192</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1008841192</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4698-7aa6c43b7e0fb4c6fb3afad9889ebc855906ba051c36717d7a7d5e7c7ef12e233</originalsourceid><addsrcrecordid>eNqNkE2P0zAQhi0EYpfCX0C5IHFJ8Fdi5wDSUkpBrArsLuJoTZyx1iVNgp2K9t_j0lKu-OKR5nln7IeQjNGCpfNqXTAlea60FAWnjBWUaq6L3QNyeW48PNeivCBPYlxTypVk9DG54JyWQgl6Sd4snEM7ZYPLboa4geB7b7Mr69ts6LPFbsTgN9hP0GXvPDQ4pe4Kx_swjDDd75-SRw66iM9O94x8e7-4m3_Irz8vP86vrnMrq1rnCqCyUjQKqWukrVwjwEFba11jY3VZ1rRqgJbMikox1SpQbYnKKnSMIxdiRl4e545h-LnFOJmNjxa7DnocttGwJEBLxmqeUH1EbRhiDOjMmL4AYZ8gc7Bn1uYgxhwkmYM988ee2aXo89OWbbPB9hz8qysBL04ARAudC9BbH_9xZcW0TGNn5PWR--U73P_3A8zb-Ze7VKV8fsz7OOHunIfww1RKqNJ8Xy0Nvf0kb5Zfb81K_Ab0eplV</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1008841192</pqid></control><display><type>article</type><title>Effect of Rosmarinic Acid on Experimental Diabetic Nephropathy</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><source>Alma/SFX Local Collection</source><creator>Jiang, Wang-Lin ; Xu, Yong ; Zhang, Shu-Ping ; Hou, Jian ; Zhu, Hai-Bo</creator><creatorcontrib>Jiang, Wang-Lin ; Xu, Yong ; Zhang, Shu-Ping ; Hou, Jian ; Zhu, Hai-Bo</creatorcontrib><description>: Connective tissue growth factor (CTGF) plays a pathogenic role in diabetic nephropathy (DN). Rosmarinic acid (RA) is a naturally occurring phenolic acid. This study was conducted to investigate the efficacy of RA on DN and to elucidate the potential mechanism. High glucose (HG)‐stimulated cultured human renal proximal tubular epithelial cells (HK‐2) analysed CTGF expression by western blotting, and it was investigated whether extracellular signal‐regulated kinase (ERK) signalling pathway was involved. Using streptozotocin (STZ)‐induced rat animal models, diabetic rats were randomized to receive intragastric (i.g.) doses of RA. Renal tissue, blood and urine samples were collected to determine biochemical index and analyse protein expression. In vitro study, RA reduced CTGF excretion in HG‐induced HK‐2 cells through the ERK signalling pathway. In an in vivo study, I.g. of RA 7.5 or 15 mg/kg significantly ameliorated renal function and increased body‐weight. Meanwhile, RA reduced renal CTGF expression by immunohistochemical staining and reduced serum levels of CTGF. Besides, there were no significant differences in glycaemia levels between the RA groups compared with the STZ‐treated group. Furthermore, RA ameliorated renal pathology. These results suggest that RA exerts an early renal protective role to DN. Inhibition of CTGF may be a potential target in DN therapy, which highlights the possibility of using RA in the treatment of DN.</description><identifier>ISSN: 1742-7835</identifier><identifier>EISSN: 1742-7843</identifier><identifier>DOI: 10.1111/j.1742-7843.2011.00828.x</identifier><identifier>PMID: 22053730</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animal models ; Animals ; Associated diseases and complications ; Biological and medical sciences ; Blood ; Body Weight - drug effects ; Cells, Cultured ; Cinnamates - administration & dosage ; Cinnamates - pharmacology ; Connective tissue growth factor ; Connective Tissue Growth Factor - metabolism ; Depsides - administration & dosage ; Depsides - pharmacology ; Diabetes mellitus ; Diabetes Mellitus, Experimental - complications ; Diabetes. Impaired glucose tolerance ; Diabetic Nephropathies - drug therapy ; Diabetic Nephropathies - pathology ; Dose-Response Relationship, Drug ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Epithelial cells ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Excretion ; Extracellular signal-regulated kinase ; Glucose ; Humans ; Kidney Tubules, Proximal - drug effects ; Kidney Tubules, Proximal - metabolism ; Kidneys ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Nephropathy ; Pharmacology. Drug treatments ; phenolic acids ; Pilot Projects ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Renal function ; Rosmarinic Acid ; Serum levels ; Signal transduction ; Streptozocin ; Urinary system involvement in other diseases. Miscellaneous ; Urine ; Western blotting</subject><ispartof>Basic & clinical pharmacology & toxicology, 2012-04, Vol.110 (4), p.390-395</ispartof><rights>2011 The Authors. Basic & Clinical Pharmacology & Toxicology © 2011 Nordic Pharmacological Society</rights><rights>2015 INIST-CNRS</rights><rights>2011 The Authors. Basic & Clinical Pharmacology & Toxicology © 2011 Nordic Pharmacological Society.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4698-7aa6c43b7e0fb4c6fb3afad9889ebc855906ba051c36717d7a7d5e7c7ef12e233</citedby><cites>FETCH-LOGICAL-c4698-7aa6c43b7e0fb4c6fb3afad9889ebc855906ba051c36717d7a7d5e7c7ef12e233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1742-7843.2011.00828.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1742-7843.2011.00828.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25618484$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22053730$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Wang-Lin</creatorcontrib><creatorcontrib>Xu, Yong</creatorcontrib><creatorcontrib>Zhang, Shu-Ping</creatorcontrib><creatorcontrib>Hou, Jian</creatorcontrib><creatorcontrib>Zhu, Hai-Bo</creatorcontrib><title>Effect of Rosmarinic Acid on Experimental Diabetic Nephropathy</title><title>Basic & clinical pharmacology & toxicology</title><addtitle>Basic Clin Pharmacol Toxicol</addtitle><description>: Connective tissue growth factor (CTGF) plays a pathogenic role in diabetic nephropathy (DN). Rosmarinic acid (RA) is a naturally occurring phenolic acid. This study was conducted to investigate the efficacy of RA on DN and to elucidate the potential mechanism. High glucose (HG)‐stimulated cultured human renal proximal tubular epithelial cells (HK‐2) analysed CTGF expression by western blotting, and it was investigated whether extracellular signal‐regulated kinase (ERK) signalling pathway was involved. Using streptozotocin (STZ)‐induced rat animal models, diabetic rats were randomized to receive intragastric (i.g.) doses of RA. Renal tissue, blood and urine samples were collected to determine biochemical index and analyse protein expression. In vitro study, RA reduced CTGF excretion in HG‐induced HK‐2 cells through the ERK signalling pathway. In an in vivo study, I.g. of RA 7.5 or 15 mg/kg significantly ameliorated renal function and increased body‐weight. Meanwhile, RA reduced renal CTGF expression by immunohistochemical staining and reduced serum levels of CTGF. Besides, there were no significant differences in glycaemia levels between the RA groups compared with the STZ‐treated group. Furthermore, RA ameliorated renal pathology. These results suggest that RA exerts an early renal protective role to DN. Inhibition of CTGF may be a potential target in DN therapy, which highlights the possibility of using RA in the treatment of DN.</description><subject>Animal models</subject><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>Blood</subject><subject>Body Weight - drug effects</subject><subject>Cells, Cultured</subject><subject>Cinnamates - administration & dosage</subject><subject>Cinnamates - pharmacology</subject><subject>Connective tissue growth factor</subject><subject>Connective Tissue Growth Factor - metabolism</subject><subject>Depsides - administration & dosage</subject><subject>Depsides - pharmacology</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - complications</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic Nephropathies - drug therapy</subject><subject>Diabetic Nephropathies - pathology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Excretion</subject><subject>Extracellular signal-regulated kinase</subject><subject>Glucose</subject><subject>Humans</subject><subject>Kidney Tubules, Proximal - drug effects</subject><subject>Kidney Tubules, Proximal - metabolism</subject><subject>Kidneys</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathy</subject><subject>Pharmacology. Drug treatments</subject><subject>phenolic acids</subject><subject>Pilot Projects</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renal function</subject><subject>Rosmarinic Acid</subject><subject>Serum levels</subject><subject>Signal transduction</subject><subject>Streptozocin</subject><subject>Urinary system involvement in other diseases. Miscellaneous</subject><subject>Urine</subject><subject>Western blotting</subject><issn>1742-7835</issn><issn>1742-7843</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE2P0zAQhi0EYpfCX0C5IHFJ8Fdi5wDSUkpBrArsLuJoTZyx1iVNgp2K9t_j0lKu-OKR5nln7IeQjNGCpfNqXTAlea60FAWnjBWUaq6L3QNyeW48PNeivCBPYlxTypVk9DG54JyWQgl6Sd4snEM7ZYPLboa4geB7b7Mr69ts6LPFbsTgN9hP0GXvPDQ4pe4Kx_swjDDd75-SRw66iM9O94x8e7-4m3_Irz8vP86vrnMrq1rnCqCyUjQKqWukrVwjwEFba11jY3VZ1rRqgJbMikox1SpQbYnKKnSMIxdiRl4e545h-LnFOJmNjxa7DnocttGwJEBLxmqeUH1EbRhiDOjMmL4AYZ8gc7Bn1uYgxhwkmYM988ee2aXo89OWbbPB9hz8qysBL04ARAudC9BbH_9xZcW0TGNn5PWR--U73P_3A8zb-Ze7VKV8fsz7OOHunIfww1RKqNJ8Xy0Nvf0kb5Zfb81K_Ab0eplV</recordid><startdate>201204</startdate><enddate>201204</enddate><creator>Jiang, Wang-Lin</creator><creator>Xu, Yong</creator><creator>Zhang, Shu-Ping</creator><creator>Hou, Jian</creator><creator>Zhu, Hai-Bo</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><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>7U7</scope><scope>C1K</scope></search><sort><creationdate>201204</creationdate><title>Effect of Rosmarinic Acid on Experimental Diabetic Nephropathy</title><author>Jiang, Wang-Lin ; Xu, Yong ; Zhang, Shu-Ping ; Hou, Jian ; Zhu, Hai-Bo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4698-7aa6c43b7e0fb4c6fb3afad9889ebc855906ba051c36717d7a7d5e7c7ef12e233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>Blood</topic><topic>Body Weight - drug effects</topic><topic>Cells, Cultured</topic><topic>Cinnamates - administration & dosage</topic><topic>Cinnamates - pharmacology</topic><topic>Connective tissue growth factor</topic><topic>Connective Tissue Growth Factor - metabolism</topic><topic>Depsides - administration & dosage</topic><topic>Depsides - pharmacology</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - complications</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetic Nephropathies - drug therapy</topic><topic>Diabetic Nephropathies - pathology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Excretion</topic><topic>Extracellular signal-regulated kinase</topic><topic>Glucose</topic><topic>Humans</topic><topic>Kidney Tubules, Proximal - drug effects</topic><topic>Kidney Tubules, Proximal - metabolism</topic><topic>Kidneys</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathy</topic><topic>Pharmacology. Drug treatments</topic><topic>phenolic acids</topic><topic>Pilot Projects</topic><topic>Random Allocation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renal function</topic><topic>Rosmarinic Acid</topic><topic>Serum levels</topic><topic>Signal transduction</topic><topic>Streptozocin</topic><topic>Urinary system involvement in other diseases. Miscellaneous</topic><topic>Urine</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Wang-Lin</creatorcontrib><creatorcontrib>Xu, Yong</creatorcontrib><creatorcontrib>Zhang, Shu-Ping</creatorcontrib><creatorcontrib>Hou, Jian</creatorcontrib><creatorcontrib>Zhu, Hai-Bo</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Basic & clinical pharmacology & toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Wang-Lin</au><au>Xu, Yong</au><au>Zhang, Shu-Ping</au><au>Hou, Jian</au><au>Zhu, Hai-Bo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Rosmarinic Acid on Experimental Diabetic Nephropathy</atitle><jtitle>Basic & clinical pharmacology & toxicology</jtitle><addtitle>Basic Clin Pharmacol Toxicol</addtitle><date>2012-04</date><risdate>2012</risdate><volume>110</volume><issue>4</issue><spage>390</spage><epage>395</epage><pages>390-395</pages><issn>1742-7835</issn><eissn>1742-7843</eissn><abstract>: Connective tissue growth factor (CTGF) plays a pathogenic role in diabetic nephropathy (DN). Rosmarinic acid (RA) is a naturally occurring phenolic acid. This study was conducted to investigate the efficacy of RA on DN and to elucidate the potential mechanism. High glucose (HG)‐stimulated cultured human renal proximal tubular epithelial cells (HK‐2) analysed CTGF expression by western blotting, and it was investigated whether extracellular signal‐regulated kinase (ERK) signalling pathway was involved. Using streptozotocin (STZ)‐induced rat animal models, diabetic rats were randomized to receive intragastric (i.g.) doses of RA. Renal tissue, blood and urine samples were collected to determine biochemical index and analyse protein expression. In vitro study, RA reduced CTGF excretion in HG‐induced HK‐2 cells through the ERK signalling pathway. In an in vivo study, I.g. of RA 7.5 or 15 mg/kg significantly ameliorated renal function and increased body‐weight. Meanwhile, RA reduced renal CTGF expression by immunohistochemical staining and reduced serum levels of CTGF. Besides, there were no significant differences in glycaemia levels between the RA groups compared with the STZ‐treated group. Furthermore, RA ameliorated renal pathology. These results suggest that RA exerts an early renal protective role to DN. Inhibition of CTGF may be a potential target in DN therapy, which highlights the possibility of using RA in the treatment of DN.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>22053730</pmid><doi>10.1111/j.1742-7843.2011.00828.x</doi><tpages>6</tpages></addata></record> |
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| subjects | Animal models Animals Associated diseases and complications Biological and medical sciences Blood Body Weight - drug effects Cells, Cultured Cinnamates - administration & dosage Cinnamates - pharmacology Connective tissue growth factor Connective Tissue Growth Factor - metabolism Depsides - administration & dosage Depsides - pharmacology Diabetes mellitus Diabetes Mellitus, Experimental - complications Diabetes. Impaired glucose tolerance Diabetic Nephropathies - drug therapy Diabetic Nephropathies - pathology Dose-Response Relationship, Drug Endocrine pancreas. Apud cells (diseases) Endocrinopathies Epithelial cells Epithelial Cells - drug effects Epithelial Cells - metabolism Etiopathogenesis. Screening. Investigations. Target tissue resistance Excretion Extracellular signal-regulated kinase Glucose Humans Kidney Tubules, Proximal - drug effects Kidney Tubules, Proximal - metabolism Kidneys Male Medical sciences Nephrology. Urinary tract diseases Nephropathy Pharmacology. Drug treatments phenolic acids Pilot Projects Random Allocation Rats Rats, Sprague-Dawley Renal function Rosmarinic Acid Serum levels Signal transduction Streptozocin Urinary system involvement in other diseases. Miscellaneous Urine Western blotting |
| title | Effect of Rosmarinic Acid on Experimental Diabetic Nephropathy |
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