Corni Fructus Alleviates UUO-Induced Renal Fibrosis via TGF-β/Smad Signaling

Renal fibrosis is a type of chronic kidney disease (CKD) induced by infiltration of inflammatory cells, myofibroblast accumulation, and ECM production in the kidney. From a long time ago, Corni Fructus (CF) is known to supplement the liver and kidney with its tepid properties. In this study, we inve...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:BioMed research international 2022, Vol.2022 (1), p.5780964-5780964
Hauptverfasser: Lee, Jin A., Shin, Mi-Rae, Roh, Seong-Soo
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 5780964
container_issue 1
container_start_page 5780964
container_title BioMed research international
container_volume 2022
creator Lee, Jin A.
Shin, Mi-Rae
Roh, Seong-Soo
description Renal fibrosis is a type of chronic kidney disease (CKD) induced by infiltration of inflammatory cells, myofibroblast accumulation, and ECM production in the kidney. From a long time ago, Corni Fructus (CF) is known to supplement the liver and kidney with its tepid properties. In this study, we investigated the renal protective mechanism of CF, which is known to supplement the kidney, in rat model of unilateral ureteral obstruction (UUO). After inducing UUO through surgery, the group was separated (n=8) and the drug was administered for 2 weeks; normal rats (normal), water-treated UUO rats (control), CF 100 mg/kg-treated UUO rats (CF100), and CF 200 mg/kg-treated UUO rats (CF200). As a result of histopathological examination of kidney tissue with H&E, MT, and PAS staining, it was confirmed that the infiltration of inflammatory cells and the erosion of collagen were relatively decreased in the kidneys treated with CF. Also, CF significantly reduced the levels of MDA and BUN in serum. As a result of confirming the expression of the factors through western blotting, CF treatment significantly reduced the expression of NADPH oxidase and significantly regulated the AMPK/LKB1/NF-κB pathway associated with inflammation. In addition, it downregulated the expression of major fibrotic signaling factors, such as α-SMA, collagen I, MMP-2, and TIMP-1, and significantly regulated the TGF-β1/Smad pathway, which is known as a major regulator of renal fibrosis. Taken together, these findings indicate that CF can alleviate renal fibrosis by regulating the TGF-β1/Smad pathway through inhibition of oxidative stress in UUO.
doi_str_mv 10.1155/2022/5780964
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9106464</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2664618213</sourcerecordid><originalsourceid>FETCH-LOGICAL-c448t-7c31d0b28e4a0d6bb996707a8feb9adf57ca4448a82d14639f81c0feb2778feb3</originalsourceid><addsrcrecordid>eNp90UFLwzAUB_Agisr05lkKXgStS9I0SS_CGFYHE0HdOaRJumV0rSat4tfyg_iZzNwc6sFcEng_HnnvD8ARghcIpWkfQ4z7KeMwo2QL7OMEkZgigrY37yTZA4fez2E4HNEAd8FekqYMM4z3we2wcbWNcteptvPRoKrMi5Wt8dFkchePat0po6N7U8sqym3hGm99FET0eJ3HH-_9h4XU0YOdhrqtpwdgp5SVN4fruwcm-dXj8CYe312PhoNxrAjhbcxUgjQsMDdEQk2LIssog0zy0hSZ1GXKlCRBSo41IjTJSo4UDEXM2NIkPXC56vvUFQujlalbJyvx5OxCujfRSCt-V2o7E9PmRWQIUkJJaHC6buCa5874ViysV6aqZG2azgtMaYpgRggM9OQPnTedC_N-KUIRx2HJPXC-UiqsyDtTbj6DoFhGJZZRiXVUgR__HGCDv4MJ4GwFZrbW8tX-3-4TJeqa7w</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2664618213</pqid></control><display><type>article</type><title>Corni Fructus Alleviates UUO-Induced Renal Fibrosis via TGF-β/Smad Signaling</title><source>MEDLINE</source><source>Wiley Online Library Open Access</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>PubMed Central Open Access</source><creator>Lee, Jin A. ; Shin, Mi-Rae ; Roh, Seong-Soo</creator><contributor>Sun, Li-kang ; Li-kang Sun</contributor><creatorcontrib>Lee, Jin A. ; Shin, Mi-Rae ; Roh, Seong-Soo ; Sun, Li-kang ; Li-kang Sun</creatorcontrib><description>Renal fibrosis is a type of chronic kidney disease (CKD) induced by infiltration of inflammatory cells, myofibroblast accumulation, and ECM production in the kidney. From a long time ago, Corni Fructus (CF) is known to supplement the liver and kidney with its tepid properties. In this study, we investigated the renal protective mechanism of CF, which is known to supplement the kidney, in rat model of unilateral ureteral obstruction (UUO). After inducing UUO through surgery, the group was separated (n=8) and the drug was administered for 2 weeks; normal rats (normal), water-treated UUO rats (control), CF 100 mg/kg-treated UUO rats (CF100), and CF 200 mg/kg-treated UUO rats (CF200). As a result of histopathological examination of kidney tissue with H&amp;E, MT, and PAS staining, it was confirmed that the infiltration of inflammatory cells and the erosion of collagen were relatively decreased in the kidneys treated with CF. Also, CF significantly reduced the levels of MDA and BUN in serum. As a result of confirming the expression of the factors through western blotting, CF treatment significantly reduced the expression of NADPH oxidase and significantly regulated the AMPK/LKB1/NF-κB pathway associated with inflammation. In addition, it downregulated the expression of major fibrotic signaling factors, such as α-SMA, collagen I, MMP-2, and TIMP-1, and significantly regulated the TGF-β1/Smad pathway, which is known as a major regulator of renal fibrosis. Taken together, these findings indicate that CF can alleviate renal fibrosis by regulating the TGF-β1/Smad pathway through inhibition of oxidative stress in UUO.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2022/5780964</identifier><identifier>PMID: 35572722</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Acids ; Animals ; Antibodies ; Apoptosis ; Collagen ; Collagen (type I) ; Cornus ; Diabetes ; Disease ; Extracellular matrix ; Fibrosis ; Gelatinase A ; Infiltration ; Inflammation ; Kidney - pathology ; Kidney diseases ; Kidney Diseases - metabolism ; Kidneys ; Liver ; LKB1 protein ; Medical research ; NAD(P)H oxidase ; NF-κB protein ; Oxidative stress ; Rats ; Renal Insufficiency, Chronic - metabolism ; Signal transduction ; Signaling ; Smad protein ; Smad Proteins - metabolism ; Solvents ; Tissue inhibitor of metalloproteinase 1 ; Transforming Growth Factor beta1 - metabolism ; Transforming growth factor-b1 ; Ureteral Obstruction - complications ; Ureteral Obstruction - drug therapy ; Ureteral Obstruction - pathology ; Western blotting</subject><ispartof>BioMed research international, 2022, Vol.2022 (1), p.5780964-5780964</ispartof><rights>Copyright © 2022 Jin A. Lee et al.</rights><rights>Copyright © 2022 Jin A. Lee et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2022 Jin A. Lee et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-7c31d0b28e4a0d6bb996707a8feb9adf57ca4448a82d14639f81c0feb2778feb3</citedby><cites>FETCH-LOGICAL-c448t-7c31d0b28e4a0d6bb996707a8feb9adf57ca4448a82d14639f81c0feb2778feb3</cites><orcidid>0000-0002-5615-4557 ; 0000-0002-4365-6988 ; 0000-0002-4162-6849</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9106464/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9106464/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35572722$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Sun, Li-kang</contributor><contributor>Li-kang Sun</contributor><creatorcontrib>Lee, Jin A.</creatorcontrib><creatorcontrib>Shin, Mi-Rae</creatorcontrib><creatorcontrib>Roh, Seong-Soo</creatorcontrib><title>Corni Fructus Alleviates UUO-Induced Renal Fibrosis via TGF-β/Smad Signaling</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Renal fibrosis is a type of chronic kidney disease (CKD) induced by infiltration of inflammatory cells, myofibroblast accumulation, and ECM production in the kidney. From a long time ago, Corni Fructus (CF) is known to supplement the liver and kidney with its tepid properties. In this study, we investigated the renal protective mechanism of CF, which is known to supplement the kidney, in rat model of unilateral ureteral obstruction (UUO). After inducing UUO through surgery, the group was separated (n=8) and the drug was administered for 2 weeks; normal rats (normal), water-treated UUO rats (control), CF 100 mg/kg-treated UUO rats (CF100), and CF 200 mg/kg-treated UUO rats (CF200). As a result of histopathological examination of kidney tissue with H&amp;E, MT, and PAS staining, it was confirmed that the infiltration of inflammatory cells and the erosion of collagen were relatively decreased in the kidneys treated with CF. Also, CF significantly reduced the levels of MDA and BUN in serum. As a result of confirming the expression of the factors through western blotting, CF treatment significantly reduced the expression of NADPH oxidase and significantly regulated the AMPK/LKB1/NF-κB pathway associated with inflammation. In addition, it downregulated the expression of major fibrotic signaling factors, such as α-SMA, collagen I, MMP-2, and TIMP-1, and significantly regulated the TGF-β1/Smad pathway, which is known as a major regulator of renal fibrosis. Taken together, these findings indicate that CF can alleviate renal fibrosis by regulating the TGF-β1/Smad pathway through inhibition of oxidative stress in UUO.</description><subject>Acids</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Cornus</subject><subject>Diabetes</subject><subject>Disease</subject><subject>Extracellular matrix</subject><subject>Fibrosis</subject><subject>Gelatinase A</subject><subject>Infiltration</subject><subject>Inflammation</subject><subject>Kidney - pathology</subject><subject>Kidney diseases</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidneys</subject><subject>Liver</subject><subject>LKB1 protein</subject><subject>Medical research</subject><subject>NAD(P)H oxidase</subject><subject>NF-κB protein</subject><subject>Oxidative stress</subject><subject>Rats</subject><subject>Renal Insufficiency, Chronic - metabolism</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Smad protein</subject><subject>Smad Proteins - metabolism</subject><subject>Solvents</subject><subject>Tissue inhibitor of metalloproteinase 1</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Transforming growth factor-b1</subject><subject>Ureteral Obstruction - complications</subject><subject>Ureteral Obstruction - drug therapy</subject><subject>Ureteral Obstruction - pathology</subject><subject>Western blotting</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp90UFLwzAUB_Agisr05lkKXgStS9I0SS_CGFYHE0HdOaRJumV0rSat4tfyg_iZzNwc6sFcEng_HnnvD8ARghcIpWkfQ4z7KeMwo2QL7OMEkZgigrY37yTZA4fez2E4HNEAd8FekqYMM4z3we2wcbWNcteptvPRoKrMi5Wt8dFkchePat0po6N7U8sqym3hGm99FET0eJ3HH-_9h4XU0YOdhrqtpwdgp5SVN4fruwcm-dXj8CYe312PhoNxrAjhbcxUgjQsMDdEQk2LIssog0zy0hSZ1GXKlCRBSo41IjTJSo4UDEXM2NIkPXC56vvUFQujlalbJyvx5OxCujfRSCt-V2o7E9PmRWQIUkJJaHC6buCa5874ViysV6aqZG2azgtMaYpgRggM9OQPnTedC_N-KUIRx2HJPXC-UiqsyDtTbj6DoFhGJZZRiXVUgR__HGCDv4MJ4GwFZrbW8tX-3-4TJeqa7w</recordid><startdate>2022</startdate><enddate>2022</enddate><creator>Lee, Jin A.</creator><creator>Shin, Mi-Rae</creator><creator>Roh, Seong-Soo</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>3V.</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</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>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5615-4557</orcidid><orcidid>https://orcid.org/0000-0002-4365-6988</orcidid><orcidid>https://orcid.org/0000-0002-4162-6849</orcidid></search><sort><creationdate>2022</creationdate><title>Corni Fructus Alleviates UUO-Induced Renal Fibrosis via TGF-β/Smad Signaling</title><author>Lee, Jin A. ; Shin, Mi-Rae ; Roh, Seong-Soo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-7c31d0b28e4a0d6bb996707a8feb9adf57ca4448a82d14639f81c0feb2778feb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acids</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Cornus</topic><topic>Diabetes</topic><topic>Disease</topic><topic>Extracellular matrix</topic><topic>Fibrosis</topic><topic>Gelatinase A</topic><topic>Infiltration</topic><topic>Inflammation</topic><topic>Kidney - pathology</topic><topic>Kidney diseases</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidneys</topic><topic>Liver</topic><topic>LKB1 protein</topic><topic>Medical research</topic><topic>NAD(P)H oxidase</topic><topic>NF-κB protein</topic><topic>Oxidative stress</topic><topic>Rats</topic><topic>Renal Insufficiency, Chronic - metabolism</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Smad protein</topic><topic>Smad Proteins - metabolism</topic><topic>Solvents</topic><topic>Tissue inhibitor of metalloproteinase 1</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Transforming growth factor-b1</topic><topic>Ureteral Obstruction - complications</topic><topic>Ureteral Obstruction - drug therapy</topic><topic>Ureteral Obstruction - pathology</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Jin A.</creatorcontrib><creatorcontrib>Shin, Mi-Rae</creatorcontrib><creatorcontrib>Roh, Seong-Soo</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><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>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Advanced Technologies &amp; Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Middle East &amp; Africa Database</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 &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Advanced Technologies &amp; Aerospace Database</collection><collection>ProQuest Advanced Technologies &amp; Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Jin A.</au><au>Shin, Mi-Rae</au><au>Roh, Seong-Soo</au><au>Sun, Li-kang</au><au>Li-kang Sun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Corni Fructus Alleviates UUO-Induced Renal Fibrosis via TGF-β/Smad Signaling</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2022</date><risdate>2022</risdate><volume>2022</volume><issue>1</issue><spage>5780964</spage><epage>5780964</epage><pages>5780964-5780964</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Renal fibrosis is a type of chronic kidney disease (CKD) induced by infiltration of inflammatory cells, myofibroblast accumulation, and ECM production in the kidney. From a long time ago, Corni Fructus (CF) is known to supplement the liver and kidney with its tepid properties. In this study, we investigated the renal protective mechanism of CF, which is known to supplement the kidney, in rat model of unilateral ureteral obstruction (UUO). After inducing UUO through surgery, the group was separated (n=8) and the drug was administered for 2 weeks; normal rats (normal), water-treated UUO rats (control), CF 100 mg/kg-treated UUO rats (CF100), and CF 200 mg/kg-treated UUO rats (CF200). As a result of histopathological examination of kidney tissue with H&amp;E, MT, and PAS staining, it was confirmed that the infiltration of inflammatory cells and the erosion of collagen were relatively decreased in the kidneys treated with CF. Also, CF significantly reduced the levels of MDA and BUN in serum. As a result of confirming the expression of the factors through western blotting, CF treatment significantly reduced the expression of NADPH oxidase and significantly regulated the AMPK/LKB1/NF-κB pathway associated with inflammation. In addition, it downregulated the expression of major fibrotic signaling factors, such as α-SMA, collagen I, MMP-2, and TIMP-1, and significantly regulated the TGF-β1/Smad pathway, which is known as a major regulator of renal fibrosis. Taken together, these findings indicate that CF can alleviate renal fibrosis by regulating the TGF-β1/Smad pathway through inhibition of oxidative stress in UUO.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>35572722</pmid><doi>10.1155/2022/5780964</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-5615-4557</orcidid><orcidid>https://orcid.org/0000-0002-4365-6988</orcidid><orcidid>https://orcid.org/0000-0002-4162-6849</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 2314-6133
ispartof BioMed research international, 2022, Vol.2022 (1), p.5780964-5780964
issn 2314-6133
2314-6141
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9106464
source MEDLINE; Wiley Online Library Open Access; PubMed Central; Alma/SFX Local Collection; PubMed Central Open Access
subjects Acids
Animals
Antibodies
Apoptosis
Collagen
Collagen (type I)
Cornus
Diabetes
Disease
Extracellular matrix
Fibrosis
Gelatinase A
Infiltration
Inflammation
Kidney - pathology
Kidney diseases
Kidney Diseases - metabolism
Kidneys
Liver
LKB1 protein
Medical research
NAD(P)H oxidase
NF-κB protein
Oxidative stress
Rats
Renal Insufficiency, Chronic - metabolism
Signal transduction
Signaling
Smad protein
Smad Proteins - metabolism
Solvents
Tissue inhibitor of metalloproteinase 1
Transforming Growth Factor beta1 - metabolism
Transforming growth factor-b1
Ureteral Obstruction - complications
Ureteral Obstruction - drug therapy
Ureteral Obstruction - pathology
Western blotting
title Corni Fructus Alleviates UUO-Induced Renal Fibrosis via TGF-β/Smad Signaling
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T05%3A53%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Corni%20Fructus%20Alleviates%20UUO-Induced%20Renal%20Fibrosis%20via%20TGF-%CE%B2/Smad%20Signaling&rft.jtitle=BioMed%20research%20international&rft.au=Lee,%20Jin%20A.&rft.date=2022&rft.volume=2022&rft.issue=1&rft.spage=5780964&rft.epage=5780964&rft.pages=5780964-5780964&rft.issn=2314-6133&rft.eissn=2314-6141&rft_id=info:doi/10.1155/2022/5780964&rft_dat=%3Cproquest_pubme%3E2664618213%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2664618213&rft_id=info:pmid/35572722&rfr_iscdi=true