Sinensetin ameliorates high glucose-induced diabetic nephropathy via enhancing autophagy in vitro and in vivo
Diabetic nephropathy (DN) affects around 40% of people with diabetes, the final outcome of which is end-stage renal disease. The deficiency of autophagy and excessive oxidative stress have been found to participate in the pathogenesis of DN. Sinensetin (SIN) has been proven to have strong antioxidan...
Gespeichert in:
Veröffentlicht in: | Journal of biochemical and molecular toxicology 2023-10, Vol.37 (10), p.e23445-e23445 |
---|---|
Hauptverfasser: | , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | e23445 |
---|---|
container_issue | 10 |
container_start_page | e23445 |
container_title | Journal of biochemical and molecular toxicology |
container_volume | 37 |
creator | Kong, Zili Lv, Wenshan Wang, Yunyang Huang, Yajing Che, Kui Nan, Huiqi Xin, Yu Wang, Jiaxuan Chen, Jintao Wang, Yangang Chi, Jingwei |
description | Diabetic nephropathy (DN) affects around 40% of people with diabetes, the final outcome of which is end-stage renal disease. The deficiency of autophagy and excessive oxidative stress have been found to participate in the pathogenesis of DN. Sinensetin (SIN) has been proven to have strong antioxidant capability. However, the effect of SIN on DN has not been studied. We examined the effect of SIN on cell viability and autophagy in the podocyte cell line, MPC5 cells, treated with high glucose (HG). For in vivo studies, DN mice models were established by intraperitoneal injected with streptozotocin (40 mg/kg) for 5 consecutive days and fed with a 60% high-fat diet, and SIN was given (10, 20, and 40 mg/kg) for 8 weeks via intraperitoneal injection. The results showed that SIN could protect MPC5 cells against HG-induced damage and significantly improve the renal function of DN mice. Moreover, SIN remarkably restored the autophagy activity of MPC5 cells which was inhibited under HG conditions. Consistent with this, SIN efficiently improved autophagy in the kidney tissue of DN mice. In brief, our findings demonstrated the protective effect of SIN on DN via restoring the autophagic function, which might provide a basis for drug development. |
doi_str_mv | 10.1002/jbt.23445 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2832577814</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2832577814</sourcerecordid><originalsourceid>FETCH-LOGICAL-c313t-df5fd6c7e98358b8c95ed873574a4ad2e2abbc9caf37978bf449cbcc0e6207093</originalsourceid><addsrcrecordid>eNpd0ctKxDAUBuAgiveFLyABN7romCZN0yxl8AYDLtR1SZPTNkOb1KQdmLe3OurCVU7g4-dwfoQuUrJICaG362pcUJZlfA8dp0TKhGR5uv898yTPBTlCJzGuCSFcCn6IjphgknFKj1H_ah24CKN1WPXQWR_UCBG3tmlx003aR0isM5MGg41V1Sw1djC0wQ9qbLd4YxUG1yqnrWuwmkY_tKrZ4jlwY8fgsXJm99n4M3RQqy7C-c97it4f7t-WT8nq5fF5ebdKNEvZmJia1ybXAmTBeFEVWnIwhWBcZCpThgJVVaWlVjUTUhRVnWVSV1oTyCkRRLJTdL3LHYL_mCCOZW-jhq5TDvwUS1owyoUo0mymV__o2k_BzdvNSrCc56kQs7rZKR18jAHqcgi2V2FbpqT86qCcOyi_O5jt5U_iVPVg_uTv0dknR_eDnA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2873656177</pqid></control><display><type>article</type><title>Sinensetin ameliorates high glucose-induced diabetic nephropathy via enhancing autophagy in vitro and in vivo</title><source>Access via Wiley Online Library</source><creator>Kong, Zili ; Lv, Wenshan ; Wang, Yunyang ; Huang, Yajing ; Che, Kui ; Nan, Huiqi ; Xin, Yu ; Wang, Jiaxuan ; Chen, Jintao ; Wang, Yangang ; Chi, Jingwei</creator><creatorcontrib>Kong, Zili ; Lv, Wenshan ; Wang, Yunyang ; Huang, Yajing ; Che, Kui ; Nan, Huiqi ; Xin, Yu ; Wang, Jiaxuan ; Chen, Jintao ; Wang, Yangang ; Chi, Jingwei</creatorcontrib><description>Diabetic nephropathy (DN) affects around 40% of people with diabetes, the final outcome of which is end-stage renal disease. The deficiency of autophagy and excessive oxidative stress have been found to participate in the pathogenesis of DN. Sinensetin (SIN) has been proven to have strong antioxidant capability. However, the effect of SIN on DN has not been studied. We examined the effect of SIN on cell viability and autophagy in the podocyte cell line, MPC5 cells, treated with high glucose (HG). For in vivo studies, DN mice models were established by intraperitoneal injected with streptozotocin (40 mg/kg) for 5 consecutive days and fed with a 60% high-fat diet, and SIN was given (10, 20, and 40 mg/kg) for 8 weeks via intraperitoneal injection. The results showed that SIN could protect MPC5 cells against HG-induced damage and significantly improve the renal function of DN mice. Moreover, SIN remarkably restored the autophagy activity of MPC5 cells which was inhibited under HG conditions. Consistent with this, SIN efficiently improved autophagy in the kidney tissue of DN mice. In brief, our findings demonstrated the protective effect of SIN on DN via restoring the autophagic function, which might provide a basis for drug development.</description><identifier>ISSN: 1095-6670</identifier><identifier>EISSN: 1099-0461</identifier><identifier>DOI: 10.1002/jbt.23445</identifier><identifier>PMID: 37393522</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Animal models ; Animal tissues ; Autophagy ; Cell viability ; Damage ; Diabetes ; Diabetes mellitus ; Diabetic nephropathy ; Drug development ; Glucose ; High fat diet ; In vivo methods and tests ; Kidneys ; Nephropathy ; Oxidative stress ; Pathogenesis ; Recovery of function ; Renal function ; Streptozocin</subject><ispartof>Journal of biochemical and molecular toxicology, 2023-10, Vol.37 (10), p.e23445-e23445</ispartof><rights>2023 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c313t-df5fd6c7e98358b8c95ed873574a4ad2e2abbc9caf37978bf449cbcc0e6207093</citedby><cites>FETCH-LOGICAL-c313t-df5fd6c7e98358b8c95ed873574a4ad2e2abbc9caf37978bf449cbcc0e6207093</cites><orcidid>0000-0001-5078-2141</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27931,27932</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37393522$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kong, Zili</creatorcontrib><creatorcontrib>Lv, Wenshan</creatorcontrib><creatorcontrib>Wang, Yunyang</creatorcontrib><creatorcontrib>Huang, Yajing</creatorcontrib><creatorcontrib>Che, Kui</creatorcontrib><creatorcontrib>Nan, Huiqi</creatorcontrib><creatorcontrib>Xin, Yu</creatorcontrib><creatorcontrib>Wang, Jiaxuan</creatorcontrib><creatorcontrib>Chen, Jintao</creatorcontrib><creatorcontrib>Wang, Yangang</creatorcontrib><creatorcontrib>Chi, Jingwei</creatorcontrib><title>Sinensetin ameliorates high glucose-induced diabetic nephropathy via enhancing autophagy in vitro and in vivo</title><title>Journal of biochemical and molecular toxicology</title><addtitle>J Biochem Mol Toxicol</addtitle><description>Diabetic nephropathy (DN) affects around 40% of people with diabetes, the final outcome of which is end-stage renal disease. The deficiency of autophagy and excessive oxidative stress have been found to participate in the pathogenesis of DN. Sinensetin (SIN) has been proven to have strong antioxidant capability. However, the effect of SIN on DN has not been studied. We examined the effect of SIN on cell viability and autophagy in the podocyte cell line, MPC5 cells, treated with high glucose (HG). For in vivo studies, DN mice models were established by intraperitoneal injected with streptozotocin (40 mg/kg) for 5 consecutive days and fed with a 60% high-fat diet, and SIN was given (10, 20, and 40 mg/kg) for 8 weeks via intraperitoneal injection. The results showed that SIN could protect MPC5 cells against HG-induced damage and significantly improve the renal function of DN mice. Moreover, SIN remarkably restored the autophagy activity of MPC5 cells which was inhibited under HG conditions. Consistent with this, SIN efficiently improved autophagy in the kidney tissue of DN mice. In brief, our findings demonstrated the protective effect of SIN on DN via restoring the autophagic function, which might provide a basis for drug development.</description><subject>Animal models</subject><subject>Animal tissues</subject><subject>Autophagy</subject><subject>Cell viability</subject><subject>Damage</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetic nephropathy</subject><subject>Drug development</subject><subject>Glucose</subject><subject>High fat diet</subject><subject>In vivo methods and tests</subject><subject>Kidneys</subject><subject>Nephropathy</subject><subject>Oxidative stress</subject><subject>Pathogenesis</subject><subject>Recovery of function</subject><subject>Renal function</subject><subject>Streptozocin</subject><issn>1095-6670</issn><issn>1099-0461</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNpd0ctKxDAUBuAgiveFLyABN7romCZN0yxl8AYDLtR1SZPTNkOb1KQdmLe3OurCVU7g4-dwfoQuUrJICaG362pcUJZlfA8dp0TKhGR5uv898yTPBTlCJzGuCSFcCn6IjphgknFKj1H_ah24CKN1WPXQWR_UCBG3tmlx003aR0isM5MGg41V1Sw1djC0wQ9qbLd4YxUG1yqnrWuwmkY_tKrZ4jlwY8fgsXJm99n4M3RQqy7C-c97it4f7t-WT8nq5fF5ebdKNEvZmJia1ybXAmTBeFEVWnIwhWBcZCpThgJVVaWlVjUTUhRVnWVSV1oTyCkRRLJTdL3LHYL_mCCOZW-jhq5TDvwUS1owyoUo0mymV__o2k_BzdvNSrCc56kQs7rZKR18jAHqcgi2V2FbpqT86qCcOyi_O5jt5U_iVPVg_uTv0dknR_eDnA</recordid><startdate>20231001</startdate><enddate>20231001</enddate><creator>Kong, Zili</creator><creator>Lv, Wenshan</creator><creator>Wang, Yunyang</creator><creator>Huang, Yajing</creator><creator>Che, Kui</creator><creator>Nan, Huiqi</creator><creator>Xin, Yu</creator><creator>Wang, Jiaxuan</creator><creator>Chen, Jintao</creator><creator>Wang, Yangang</creator><creator>Chi, Jingwei</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5078-2141</orcidid></search><sort><creationdate>20231001</creationdate><title>Sinensetin ameliorates high glucose-induced diabetic nephropathy via enhancing autophagy in vitro and in vivo</title><author>Kong, Zili ; Lv, Wenshan ; Wang, Yunyang ; Huang, Yajing ; Che, Kui ; Nan, Huiqi ; Xin, Yu ; Wang, Jiaxuan ; Chen, Jintao ; Wang, Yangang ; Chi, Jingwei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c313t-df5fd6c7e98358b8c95ed873574a4ad2e2abbc9caf37978bf449cbcc0e6207093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animal models</topic><topic>Animal tissues</topic><topic>Autophagy</topic><topic>Cell viability</topic><topic>Damage</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetic nephropathy</topic><topic>Drug development</topic><topic>Glucose</topic><topic>High fat diet</topic><topic>In vivo methods and tests</topic><topic>Kidneys</topic><topic>Nephropathy</topic><topic>Oxidative stress</topic><topic>Pathogenesis</topic><topic>Recovery of function</topic><topic>Renal function</topic><topic>Streptozocin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kong, Zili</creatorcontrib><creatorcontrib>Lv, Wenshan</creatorcontrib><creatorcontrib>Wang, Yunyang</creatorcontrib><creatorcontrib>Huang, Yajing</creatorcontrib><creatorcontrib>Che, Kui</creatorcontrib><creatorcontrib>Nan, Huiqi</creatorcontrib><creatorcontrib>Xin, Yu</creatorcontrib><creatorcontrib>Wang, Jiaxuan</creatorcontrib><creatorcontrib>Chen, Jintao</creatorcontrib><creatorcontrib>Wang, Yangang</creatorcontrib><creatorcontrib>Chi, Jingwei</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biochemical and molecular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kong, Zili</au><au>Lv, Wenshan</au><au>Wang, Yunyang</au><au>Huang, Yajing</au><au>Che, Kui</au><au>Nan, Huiqi</au><au>Xin, Yu</au><au>Wang, Jiaxuan</au><au>Chen, Jintao</au><au>Wang, Yangang</au><au>Chi, Jingwei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sinensetin ameliorates high glucose-induced diabetic nephropathy via enhancing autophagy in vitro and in vivo</atitle><jtitle>Journal of biochemical and molecular toxicology</jtitle><addtitle>J Biochem Mol Toxicol</addtitle><date>2023-10-01</date><risdate>2023</risdate><volume>37</volume><issue>10</issue><spage>e23445</spage><epage>e23445</epage><pages>e23445-e23445</pages><issn>1095-6670</issn><eissn>1099-0461</eissn><abstract>Diabetic nephropathy (DN) affects around 40% of people with diabetes, the final outcome of which is end-stage renal disease. The deficiency of autophagy and excessive oxidative stress have been found to participate in the pathogenesis of DN. Sinensetin (SIN) has been proven to have strong antioxidant capability. However, the effect of SIN on DN has not been studied. We examined the effect of SIN on cell viability and autophagy in the podocyte cell line, MPC5 cells, treated with high glucose (HG). For in vivo studies, DN mice models were established by intraperitoneal injected with streptozotocin (40 mg/kg) for 5 consecutive days and fed with a 60% high-fat diet, and SIN was given (10, 20, and 40 mg/kg) for 8 weeks via intraperitoneal injection. The results showed that SIN could protect MPC5 cells against HG-induced damage and significantly improve the renal function of DN mice. Moreover, SIN remarkably restored the autophagy activity of MPC5 cells which was inhibited under HG conditions. Consistent with this, SIN efficiently improved autophagy in the kidney tissue of DN mice. In brief, our findings demonstrated the protective effect of SIN on DN via restoring the autophagic function, which might provide a basis for drug development.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>37393522</pmid><doi>10.1002/jbt.23445</doi><orcidid>https://orcid.org/0000-0001-5078-2141</orcidid></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1095-6670 |
ispartof | Journal of biochemical and molecular toxicology, 2023-10, Vol.37 (10), p.e23445-e23445 |
issn | 1095-6670 1099-0461 |
language | eng |
recordid | cdi_proquest_miscellaneous_2832577814 |
source | Access via Wiley Online Library |
subjects | Animal models Animal tissues Autophagy Cell viability Damage Diabetes Diabetes mellitus Diabetic nephropathy Drug development Glucose High fat diet In vivo methods and tests Kidneys Nephropathy Oxidative stress Pathogenesis Recovery of function Renal function Streptozocin |
title | Sinensetin ameliorates high glucose-induced diabetic nephropathy via enhancing autophagy in vitro and in vivo |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-05T14%3A56%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Sinensetin%20ameliorates%20high%20glucose-induced%20diabetic%20nephropathy%20via%20enhancing%20autophagy%20in%20vitro%20and%20in%20vivo&rft.jtitle=Journal%20of%20biochemical%20and%20molecular%20toxicology&rft.au=Kong,%20Zili&rft.date=2023-10-01&rft.volume=37&rft.issue=10&rft.spage=e23445&rft.epage=e23445&rft.pages=e23445-e23445&rft.issn=1095-6670&rft.eissn=1099-0461&rft_id=info:doi/10.1002/jbt.23445&rft_dat=%3Cproquest_cross%3E2832577814%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2873656177&rft_id=info:pmid/37393522&rfr_iscdi=true |