Ligustrazine suppresses renal NMDAR1 and caspase-3 expressions in a mouse model of sepsis-associated acute kidney injury
Sepsis-associated acute kidney injury (AKI) is a life threatening condition with high morbidity and mortality. The pathogenesis of AKI is associated with apoptosis. In this study, we investigated the effects of ligustrazine (LGZ) on experimental sepsis-associated AKI in mice. Sepsis-associated AKI w...
Gespeichert in:
Veröffentlicht in: | Molecular and cellular biochemistry 2020, Vol.464 (1-2), p.73-81 |
---|---|
Hauptverfasser: | , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 81 |
---|---|
container_issue | 1-2 |
container_start_page | 73 |
container_title | Molecular and cellular biochemistry |
container_volume | 464 |
creator | Ying, Jing Wu, Jin Zhang, Yiwei Han, Yangyang Qian, Xinger Yang, Qiuhong Chen, Yongjie Chen, Yijun Zhu, Hao |
description | Sepsis-associated acute kidney injury (AKI) is a life threatening condition with high morbidity and mortality. The pathogenesis of AKI is associated with apoptosis. In this study, we investigated the effects of ligustrazine (LGZ) on experimental sepsis-associated AKI in mice. Sepsis-associated AKI was induced in a mice model using cecal ligation and puncture (CLP) method. Mice were administered LGZ (10, 30, and 60 mg/kg) via tail vein injection 0.5 h before CLP surgery. Mice survival was evaluated. Renal water content was detected. Urine samples were collected for ELISA of Kim1. Kidneys were collected for nucleic acid analysis and histological examination. Pathological assessment was used to determine the effect of LGZ on sepsis-associated AKI. Caspase-3 expression in kidney was assessed by immunohistochemistry. Renal NMDAR1 level was also determined. Treatment of LGZ improved mice survival rate; the effect was significant when administered at a high LGZ dose (60 mg/kg). Renal water content of mice undergoing CLP was significantly reduced by LGZ treatment. Both middle-dose and high-dose LGZ treatments reduced urine Kim1 level in sepsis-associated AKI mice. The severity of AKI in septic mice was reduced by middle-dose and high-dose LGZ administration. Immunohistochemical analysis revealed decreased caspase-3 and NMDAR1 levels in the kidney following middle-dose and high-dose LGZ treatments. RT-PCR assay showed a significant reduction in NMDAR1 mRNA expression in the kidney of middle-dose and high-dose LGZ-treated mice. LGZ exhibited protective effects against sepsis-associated AKI in mice, possibly via downregulation of renal NMDAR1 expression and its anti-apoptotic action by inhibiting caspase-3. |
doi_str_mv | 10.1007/s11010-019-03650-4 |
format | Article |
fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2315103782</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A610874387</galeid><sourcerecordid>A610874387</sourcerecordid><originalsourceid>FETCH-LOGICAL-c442t-59442ccbb9c8968aec9dde26ae708afde5c2b2e7259aaf35758c4e90f989b68b3</originalsourceid><addsrcrecordid>eNp9kU-LFDEQxRtR3HH1C3iQgBcvWfOn00mOw-qqMCqInkM6XT1k7Em3qW7Y8dNvZmd1UUQCKaj83qNSr6qec3bBGdOvkXPGGWXcUiYbxWj9oFpxpSWtLbcPqxWTjFHDtT6rniDuWKEZ54-rM8m1FEaKVXW9idsF5-x_xgQEl2nKgAhIMiQ_kE8f36y_cOJTR4LHySNQSeD6FopjQhIT8WQ_Lgjl7mAgY08QJoxIPeIYop-hIz4sM5DvsUtwKJLdkg9Pq0e9HxCe3dXz6tvV26-X7-nm87sPl-sNDXUtZqpsKSG0rQ3GNsZDsF0HovGgmfF9ByqIVoAWynrfS6WVCTVY1ltj28a08rx6dfKd8vhjAZzdPmKAYfAJythOSK44k9qIgr78C92NSy5rOFK1lExYpe6prR_AxdSPZXvhaOrWDWdG19LoQl38gyqng30MY4I-lv4fAnEShDwiZujdlOPe54PjzB3jdqe4XYnb3cbt6iJ6cTfx0u6h-y35lW8B5AnA8pS2kO-_9B_bGw11tLs</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2343302955</pqid></control><display><type>article</type><title>Ligustrazine suppresses renal NMDAR1 and caspase-3 expressions in a mouse model of sepsis-associated acute kidney injury</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Ying, Jing ; Wu, Jin ; Zhang, Yiwei ; Han, Yangyang ; Qian, Xinger ; Yang, Qiuhong ; Chen, Yongjie ; Chen, Yijun ; Zhu, Hao</creator><creatorcontrib>Ying, Jing ; Wu, Jin ; Zhang, Yiwei ; Han, Yangyang ; Qian, Xinger ; Yang, Qiuhong ; Chen, Yongjie ; Chen, Yijun ; Zhu, Hao</creatorcontrib><description>Sepsis-associated acute kidney injury (AKI) is a life threatening condition with high morbidity and mortality. The pathogenesis of AKI is associated with apoptosis. In this study, we investigated the effects of ligustrazine (LGZ) on experimental sepsis-associated AKI in mice. Sepsis-associated AKI was induced in a mice model using cecal ligation and puncture (CLP) method. Mice were administered LGZ (10, 30, and 60 mg/kg) via tail vein injection 0.5 h before CLP surgery. Mice survival was evaluated. Renal water content was detected. Urine samples were collected for ELISA of Kim1. Kidneys were collected for nucleic acid analysis and histological examination. Pathological assessment was used to determine the effect of LGZ on sepsis-associated AKI. Caspase-3 expression in kidney was assessed by immunohistochemistry. Renal NMDAR1 level was also determined. Treatment of LGZ improved mice survival rate; the effect was significant when administered at a high LGZ dose (60 mg/kg). Renal water content of mice undergoing CLP was significantly reduced by LGZ treatment. Both middle-dose and high-dose LGZ treatments reduced urine Kim1 level in sepsis-associated AKI mice. The severity of AKI in septic mice was reduced by middle-dose and high-dose LGZ administration. Immunohistochemical analysis revealed decreased caspase-3 and NMDAR1 levels in the kidney following middle-dose and high-dose LGZ treatments. RT-PCR assay showed a significant reduction in NMDAR1 mRNA expression in the kidney of middle-dose and high-dose LGZ-treated mice. LGZ exhibited protective effects against sepsis-associated AKI in mice, possibly via downregulation of renal NMDAR1 expression and its anti-apoptotic action by inhibiting caspase-3.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-019-03650-4</identifier><identifier>PMID: 31732832</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acute Kidney Injury - drug therapy ; Acute Kidney Injury - metabolism ; Acute Kidney Injury - pathology ; Analysis ; Animals ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Caspase 3 - biosynthesis ; Caspase-3 ; Cecum ; Disease Models, Animal ; Dosage ; Enzyme-linked immunosorbent assay ; Gene expression ; Gene Expression Regulation - drug effects ; Glutamate receptors ; Health aspects ; Immunohistochemistry ; Infection ; Kidneys ; Life Sciences ; Male ; Medical Biochemistry ; Mice ; Moisture content ; Morbidity ; N-Methyl-D-aspartic acid receptors ; Nucleic acids ; Oncology ; Pathogenesis ; Polymerase chain reaction ; Pyrazines - pharmacology ; Receptors, N-Methyl-D-Aspartate - biosynthesis ; RNA ; Sepsis ; Sepsis - drug therapy ; Sepsis - metabolism ; Sepsis - pathology ; Surgery ; Survival ; Urine ; Water content</subject><ispartof>Molecular and cellular biochemistry, 2020, Vol.464 (1-2), p.73-81</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>COPYRIGHT 2020 Springer</rights><rights>Molecular and Cellular Biochemistry is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-59442ccbb9c8968aec9dde26ae708afde5c2b2e7259aaf35758c4e90f989b68b3</citedby><cites>FETCH-LOGICAL-c442t-59442ccbb9c8968aec9dde26ae708afde5c2b2e7259aaf35758c4e90f989b68b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-019-03650-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-019-03650-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,41471,42540,51302</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31732832$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ying, Jing</creatorcontrib><creatorcontrib>Wu, Jin</creatorcontrib><creatorcontrib>Zhang, Yiwei</creatorcontrib><creatorcontrib>Han, Yangyang</creatorcontrib><creatorcontrib>Qian, Xinger</creatorcontrib><creatorcontrib>Yang, Qiuhong</creatorcontrib><creatorcontrib>Chen, Yongjie</creatorcontrib><creatorcontrib>Chen, Yijun</creatorcontrib><creatorcontrib>Zhu, Hao</creatorcontrib><title>Ligustrazine suppresses renal NMDAR1 and caspase-3 expressions in a mouse model of sepsis-associated acute kidney injury</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Sepsis-associated acute kidney injury (AKI) is a life threatening condition with high morbidity and mortality. The pathogenesis of AKI is associated with apoptosis. In this study, we investigated the effects of ligustrazine (LGZ) on experimental sepsis-associated AKI in mice. Sepsis-associated AKI was induced in a mice model using cecal ligation and puncture (CLP) method. Mice were administered LGZ (10, 30, and 60 mg/kg) via tail vein injection 0.5 h before CLP surgery. Mice survival was evaluated. Renal water content was detected. Urine samples were collected for ELISA of Kim1. Kidneys were collected for nucleic acid analysis and histological examination. Pathological assessment was used to determine the effect of LGZ on sepsis-associated AKI. Caspase-3 expression in kidney was assessed by immunohistochemistry. Renal NMDAR1 level was also determined. Treatment of LGZ improved mice survival rate; the effect was significant when administered at a high LGZ dose (60 mg/kg). Renal water content of mice undergoing CLP was significantly reduced by LGZ treatment. Both middle-dose and high-dose LGZ treatments reduced urine Kim1 level in sepsis-associated AKI mice. The severity of AKI in septic mice was reduced by middle-dose and high-dose LGZ administration. Immunohistochemical analysis revealed decreased caspase-3 and NMDAR1 levels in the kidney following middle-dose and high-dose LGZ treatments. RT-PCR assay showed a significant reduction in NMDAR1 mRNA expression in the kidney of middle-dose and high-dose LGZ-treated mice. LGZ exhibited protective effects against sepsis-associated AKI in mice, possibly via downregulation of renal NMDAR1 expression and its anti-apoptotic action by inhibiting caspase-3.</description><subject>Acute Kidney Injury - drug therapy</subject><subject>Acute Kidney Injury - metabolism</subject><subject>Acute Kidney Injury - pathology</subject><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Caspase 3 - biosynthesis</subject><subject>Caspase-3</subject><subject>Cecum</subject><subject>Disease Models, Animal</subject><subject>Dosage</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glutamate receptors</subject><subject>Health aspects</subject><subject>Immunohistochemistry</subject><subject>Infection</subject><subject>Kidneys</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Medical Biochemistry</subject><subject>Mice</subject><subject>Moisture content</subject><subject>Morbidity</subject><subject>N-Methyl-D-aspartic acid receptors</subject><subject>Nucleic acids</subject><subject>Oncology</subject><subject>Pathogenesis</subject><subject>Polymerase chain reaction</subject><subject>Pyrazines - pharmacology</subject><subject>Receptors, N-Methyl-D-Aspartate - biosynthesis</subject><subject>RNA</subject><subject>Sepsis</subject><subject>Sepsis - drug therapy</subject><subject>Sepsis - metabolism</subject><subject>Sepsis - pathology</subject><subject>Surgery</subject><subject>Survival</subject><subject>Urine</subject><subject>Water content</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</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>eNp9kU-LFDEQxRtR3HH1C3iQgBcvWfOn00mOw-qqMCqInkM6XT1k7Em3qW7Y8dNvZmd1UUQCKaj83qNSr6qec3bBGdOvkXPGGWXcUiYbxWj9oFpxpSWtLbcPqxWTjFHDtT6rniDuWKEZ54-rM8m1FEaKVXW9idsF5-x_xgQEl2nKgAhIMiQ_kE8f36y_cOJTR4LHySNQSeD6FopjQhIT8WQ_Lgjl7mAgY08QJoxIPeIYop-hIz4sM5DvsUtwKJLdkg9Pq0e9HxCe3dXz6tvV26-X7-nm87sPl-sNDXUtZqpsKSG0rQ3GNsZDsF0HovGgmfF9ByqIVoAWynrfS6WVCTVY1ltj28a08rx6dfKd8vhjAZzdPmKAYfAJythOSK44k9qIgr78C92NSy5rOFK1lExYpe6prR_AxdSPZXvhaOrWDWdG19LoQl38gyqng30MY4I-lv4fAnEShDwiZujdlOPe54PjzB3jdqe4XYnb3cbt6iJ6cTfx0u6h-y35lW8B5AnA8pS2kO-_9B_bGw11tLs</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Ying, Jing</creator><creator>Wu, Jin</creator><creator>Zhang, Yiwei</creator><creator>Han, Yangyang</creator><creator>Qian, Xinger</creator><creator>Yang, Qiuhong</creator><creator>Chen, Yongjie</creator><creator>Chen, Yijun</creator><creator>Zhu, Hao</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>2020</creationdate><title>Ligustrazine suppresses renal NMDAR1 and caspase-3 expressions in a mouse model of sepsis-associated acute kidney injury</title><author>Ying, Jing ; Wu, Jin ; Zhang, Yiwei ; Han, Yangyang ; Qian, Xinger ; Yang, Qiuhong ; Chen, Yongjie ; Chen, Yijun ; Zhu, Hao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-59442ccbb9c8968aec9dde26ae708afde5c2b2e7259aaf35758c4e90f989b68b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acute Kidney Injury - drug therapy</topic><topic>Acute Kidney Injury - metabolism</topic><topic>Acute Kidney Injury - pathology</topic><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiology</topic><topic>Caspase 3 - biosynthesis</topic><topic>Caspase-3</topic><topic>Cecum</topic><topic>Disease Models, Animal</topic><topic>Dosage</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Glutamate receptors</topic><topic>Health aspects</topic><topic>Immunohistochemistry</topic><topic>Infection</topic><topic>Kidneys</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Medical Biochemistry</topic><topic>Mice</topic><topic>Moisture content</topic><topic>Morbidity</topic><topic>N-Methyl-D-aspartic acid receptors</topic><topic>Nucleic acids</topic><topic>Oncology</topic><topic>Pathogenesis</topic><topic>Polymerase chain reaction</topic><topic>Pyrazines - pharmacology</topic><topic>Receptors, N-Methyl-D-Aspartate - biosynthesis</topic><topic>RNA</topic><topic>Sepsis</topic><topic>Sepsis - drug therapy</topic><topic>Sepsis - metabolism</topic><topic>Sepsis - pathology</topic><topic>Surgery</topic><topic>Survival</topic><topic>Urine</topic><topic>Water content</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ying, Jing</creatorcontrib><creatorcontrib>Wu, Jin</creatorcontrib><creatorcontrib>Zhang, Yiwei</creatorcontrib><creatorcontrib>Han, Yangyang</creatorcontrib><creatorcontrib>Qian, Xinger</creatorcontrib><creatorcontrib>Yang, Qiuhong</creatorcontrib><creatorcontrib>Chen, Yongjie</creatorcontrib><creatorcontrib>Chen, Yijun</creatorcontrib><creatorcontrib>Zhu, Hao</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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 One Sustainability</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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</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>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ying, Jing</au><au>Wu, Jin</au><au>Zhang, Yiwei</au><au>Han, Yangyang</au><au>Qian, Xinger</au><au>Yang, Qiuhong</au><au>Chen, Yongjie</au><au>Chen, Yijun</au><au>Zhu, Hao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ligustrazine suppresses renal NMDAR1 and caspase-3 expressions in a mouse model of sepsis-associated acute kidney injury</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2020</date><risdate>2020</risdate><volume>464</volume><issue>1-2</issue><spage>73</spage><epage>81</epage><pages>73-81</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Sepsis-associated acute kidney injury (AKI) is a life threatening condition with high morbidity and mortality. The pathogenesis of AKI is associated with apoptosis. In this study, we investigated the effects of ligustrazine (LGZ) on experimental sepsis-associated AKI in mice. Sepsis-associated AKI was induced in a mice model using cecal ligation and puncture (CLP) method. Mice were administered LGZ (10, 30, and 60 mg/kg) via tail vein injection 0.5 h before CLP surgery. Mice survival was evaluated. Renal water content was detected. Urine samples were collected for ELISA of Kim1. Kidneys were collected for nucleic acid analysis and histological examination. Pathological assessment was used to determine the effect of LGZ on sepsis-associated AKI. Caspase-3 expression in kidney was assessed by immunohistochemistry. Renal NMDAR1 level was also determined. Treatment of LGZ improved mice survival rate; the effect was significant when administered at a high LGZ dose (60 mg/kg). Renal water content of mice undergoing CLP was significantly reduced by LGZ treatment. Both middle-dose and high-dose LGZ treatments reduced urine Kim1 level in sepsis-associated AKI mice. The severity of AKI in septic mice was reduced by middle-dose and high-dose LGZ administration. Immunohistochemical analysis revealed decreased caspase-3 and NMDAR1 levels in the kidney following middle-dose and high-dose LGZ treatments. RT-PCR assay showed a significant reduction in NMDAR1 mRNA expression in the kidney of middle-dose and high-dose LGZ-treated mice. LGZ exhibited protective effects against sepsis-associated AKI in mice, possibly via downregulation of renal NMDAR1 expression and its anti-apoptotic action by inhibiting caspase-3.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>31732832</pmid><doi>10.1007/s11010-019-03650-4</doi><tpages>9</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0300-8177 |
ispartof | Molecular and cellular biochemistry, 2020, Vol.464 (1-2), p.73-81 |
issn | 0300-8177 1573-4919 |
language | eng |
recordid | cdi_proquest_miscellaneous_2315103782 |
source | MEDLINE; SpringerLink Journals - AutoHoldings |
subjects | Acute Kidney Injury - drug therapy Acute Kidney Injury - metabolism Acute Kidney Injury - pathology Analysis Animals Apoptosis Biochemistry Biomedical and Life Sciences Cardiology Caspase 3 - biosynthesis Caspase-3 Cecum Disease Models, Animal Dosage Enzyme-linked immunosorbent assay Gene expression Gene Expression Regulation - drug effects Glutamate receptors Health aspects Immunohistochemistry Infection Kidneys Life Sciences Male Medical Biochemistry Mice Moisture content Morbidity N-Methyl-D-aspartic acid receptors Nucleic acids Oncology Pathogenesis Polymerase chain reaction Pyrazines - pharmacology Receptors, N-Methyl-D-Aspartate - biosynthesis RNA Sepsis Sepsis - drug therapy Sepsis - metabolism Sepsis - pathology Surgery Survival Urine Water content |
title | Ligustrazine suppresses renal NMDAR1 and caspase-3 expressions in a mouse model of sepsis-associated acute kidney injury |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T19%3A14%3A46IST&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=Ligustrazine%20suppresses%20renal%20NMDAR1%20and%20caspase-3%20expressions%20in%20a%20mouse%20model%20of%20sepsis-associated%20acute%20kidney%20injury&rft.jtitle=Molecular%20and%20cellular%20biochemistry&rft.au=Ying,%20Jing&rft.date=2020&rft.volume=464&rft.issue=1-2&rft.spage=73&rft.epage=81&rft.pages=73-81&rft.issn=0300-8177&rft.eissn=1573-4919&rft_id=info:doi/10.1007/s11010-019-03650-4&rft_dat=%3Cgale_proqu%3EA610874387%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=2343302955&rft_id=info:pmid/31732832&rft_galeid=A610874387&rfr_iscdi=true |