Ischemic postconditioning protects against acute kidney injury after limb ischemia reperfusion by regulating HMGB1 release and autophagy
Ischemic postconditioning (I-PostC) has a protective effect against acute kidney injury (AKI) induced by limb ischemia-reperfusion (LIR); however, the exact mechanism remains to be elucidated. Our study aims to investigate the potential involvement of high-mobility group box 1 protein (HMGB1) and au...
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| description | Ischemic postconditioning (I-PostC) has a protective effect against acute kidney injury (AKI) induced by limb ischemia-reperfusion (LIR); however, the exact mechanism remains to be elucidated. Our study aims to investigate the potential involvement of high-mobility group box 1 protein (HMGB1) and autophagy in renoprotection generated by I-PostC. A rat model of LIR-induced AKI was established and rats were randomly assigned to five groups: (i) sham-operated control, (ii) I/R, (iii) I/R + I-PostC, (iv) I/R + I-PostC + rapamycin (autophagy activator), and (v) I/R + I-PostC + 3-methyladenine (autophagy inhibitor). Morphological changes in the kidneys were assessed by histology, and ultrastructural changes in renal tubular epithelial cells and glomerular podocytes were observed by transmission electron microscopy. The levels of kidney function parameters, serum inflammatory factors, and autophagy markers were detected. The results showed that the levels of HMGB1, Beclin1, LC3-II/LC3-I, and inflammatory cytokines (TNF-α and IL-6) were significantly higher in the I/R group compared to the sham control in serum and in renal tissues. I-PostC significantly reduced the levels of HMGB1, Beclin1, LC3-II/LC3-I, and inflammatory cytokines in renal tissues and improved renal function. Renal histopathology and ultrastructural observations indicated that I-PostC alleviated renal tissue injury. In addition, rapamycin (autophagy activator) treatment increased the levels of inflammatory cytokine expression levels and decreased renal function, reversed the protective effect of I-PostC against LIR-induced AKI. In conclusion, I-PostC could play a protective role against AKI by regulating the release of HMGB1 and inhibiting autophagy activation. |
| doi_str_mv | 10.1080/0886022X.2023.2189482 |
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Our study aims to investigate the potential involvement of high-mobility group box 1 protein (HMGB1) and autophagy in renoprotection generated by I-PostC. A rat model of LIR-induced AKI was established and rats were randomly assigned to five groups: (i) sham-operated control, (ii) I/R, (iii) I/R + I-PostC, (iv) I/R + I-PostC + rapamycin (autophagy activator), and (v) I/R + I-PostC + 3-methyladenine (autophagy inhibitor). Morphological changes in the kidneys were assessed by histology, and ultrastructural changes in renal tubular epithelial cells and glomerular podocytes were observed by transmission electron microscopy. The levels of kidney function parameters, serum inflammatory factors, and autophagy markers were detected. The results showed that the levels of HMGB1, Beclin1, LC3-II/LC3-I, and inflammatory cytokines (TNF-α and IL-6) were significantly higher in the I/R group compared to the sham control in serum and in renal tissues. I-PostC significantly reduced the levels of HMGB1, Beclin1, LC3-II/LC3-I, and inflammatory cytokines in renal tissues and improved renal function. Renal histopathology and ultrastructural observations indicated that I-PostC alleviated renal tissue injury. In addition, rapamycin (autophagy activator) treatment increased the levels of inflammatory cytokine expression levels and decreased renal function, reversed the protective effect of I-PostC against LIR-induced AKI. In conclusion, I-PostC could play a protective role against AKI by regulating the release of HMGB1 and inhibiting autophagy activation.</description><identifier>ISSN: 0886-022X</identifier><identifier>EISSN: 1525-6049</identifier><identifier>DOI: 10.1080/0886022X.2023.2189482</identifier><identifier>PMID: 37158301</identifier><language>eng</language><publisher>England: Taylor & Francis</publisher><subject>Acute Kidney Injury - etiology ; Acute Kidney Injury - prevention & control ; Animals ; Autophagy ; Beclin-1 - metabolism ; Clinical Study ; Cytokines ; Epithelial cells ; HMGB1 ; HMGB1 Protein ; Inflammation ; Ischemia ; ischemic postconditioning ; Ischemic Postconditioning - methods ; kidney ; Kidneys ; Limb ischemia ; Rapamycin ; Rats ; Renal function ; Reperfusion ; Reperfusion Injury - complications ; Reperfusion Injury - prevention & control ; Sirolimus - pharmacology ; Transmission electron microscopy ; Tumor necrosis factor-α</subject><ispartof>Renal failure, 2023-12, Vol.45 (1), p.2189482-2189482</ispartof><rights>2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2023</rights><rights>2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2023 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c511t-c52bd502411e00536bc152a2bc8f7f8ff585c3bae1c90fed706747fb552b25dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10171135/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10171135/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,27502,27924,27925,53791,53793,59143,59144</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37158301$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Zhongdi</creatorcontrib><creatorcontrib>Chen, Yifan</creatorcontrib><creatorcontrib>Du, Zhe</creatorcontrib><creatorcontrib>Zhu, Fengxue</creatorcontrib><creatorcontrib>Huang, Wei</creatorcontrib><title>Ischemic postconditioning protects against acute kidney injury after limb ischemia reperfusion by regulating HMGB1 release and autophagy</title><title>Renal failure</title><addtitle>Ren Fail</addtitle><description>Ischemic postconditioning (I-PostC) has a protective effect against acute kidney injury (AKI) induced by limb ischemia-reperfusion (LIR); however, the exact mechanism remains to be elucidated. Our study aims to investigate the potential involvement of high-mobility group box 1 protein (HMGB1) and autophagy in renoprotection generated by I-PostC. A rat model of LIR-induced AKI was established and rats were randomly assigned to five groups: (i) sham-operated control, (ii) I/R, (iii) I/R + I-PostC, (iv) I/R + I-PostC + rapamycin (autophagy activator), and (v) I/R + I-PostC + 3-methyladenine (autophagy inhibitor). Morphological changes in the kidneys were assessed by histology, and ultrastructural changes in renal tubular epithelial cells and glomerular podocytes were observed by transmission electron microscopy. The levels of kidney function parameters, serum inflammatory factors, and autophagy markers were detected. The results showed that the levels of HMGB1, Beclin1, LC3-II/LC3-I, and inflammatory cytokines (TNF-α and IL-6) were significantly higher in the I/R group compared to the sham control in serum and in renal tissues. I-PostC significantly reduced the levels of HMGB1, Beclin1, LC3-II/LC3-I, and inflammatory cytokines in renal tissues and improved renal function. Renal histopathology and ultrastructural observations indicated that I-PostC alleviated renal tissue injury. In addition, rapamycin (autophagy activator) treatment increased the levels of inflammatory cytokine expression levels and decreased renal function, reversed the protective effect of I-PostC against LIR-induced AKI. In conclusion, I-PostC could play a protective role against AKI by regulating the release of HMGB1 and inhibiting autophagy activation.</description><subject>Acute Kidney Injury - etiology</subject><subject>Acute Kidney Injury - prevention & control</subject><subject>Animals</subject><subject>Autophagy</subject><subject>Beclin-1 - metabolism</subject><subject>Clinical Study</subject><subject>Cytokines</subject><subject>Epithelial cells</subject><subject>HMGB1</subject><subject>HMGB1 Protein</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>ischemic postconditioning</subject><subject>Ischemic Postconditioning - methods</subject><subject>kidney</subject><subject>Kidneys</subject><subject>Limb ischemia</subject><subject>Rapamycin</subject><subject>Rats</subject><subject>Renal function</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - complications</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Sirolimus - pharmacology</subject><subject>Transmission electron microscopy</subject><subject>Tumor necrosis factor-α</subject><issn>0886-022X</issn><issn>1525-6049</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><sourceid>DOA</sourceid><recordid>eNp9ks9u1DAQxiMEokvhEUCWuHDZxePEm-QEpYJ2pSIuIHGzHGec9ZLYwXZAeQMeG4fdVpQDF_8Zf_Mbj_1l2XOgG6AVfU2raksZ-7phlOUbBlVdVOxBtgLO-HpLi_phtlo060V0lj0J4UAp8Kpkj7OzvEyrnMIq-7ULao-DUWR0ISpnWxONs8Z2ZPQuooqByE4aGyKRaopIvpnW4kyMPUx-JlJH9KQ3Q0PMkSSJxxG9nkLikGZO227qZVyQ1x-v3kEK9CgDEmlbIqfoxr3s5qfZIy37gM9O83n25cP7z5fX65tPV7vLi5u14gAxjaxpOWUFAFLK822jUseSNarSpa605hVXeSMRVE01tiXdlkWpG57yGG9Vfp7tjtzWyYMYvRmkn4WTRvwJON8J6aNRPQpWcw25qlHlWKDiDbClItTAFTbbJrHeHFnj1AzYKrTRy_4e9P6JNXvRuR8CKJQAOU-EVyeCd98nDFEM6Rmx76VFNwXBKgBe0qKskvTlP9KDm7xNb5VU6T8hr_kC5EeV8i4Ej_ruNkDFYhxxaxyxGEecjJPyXvzdyl3WrVOS4O1RYKx2fpA_ne9bEeXcO6-9tMoEkf-_xm8IBdW7</recordid><startdate>202312</startdate><enddate>202312</enddate><creator>Liu, Zhongdi</creator><creator>Chen, Yifan</creator><creator>Du, Zhe</creator><creator>Zhu, Fengxue</creator><creator>Huang, Wei</creator><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><general>Taylor & Francis Group</general><scope>0YH</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>7T5</scope><scope>7XB</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>202312</creationdate><title>Ischemic postconditioning protects against acute kidney injury after limb ischemia reperfusion by regulating HMGB1 release and autophagy</title><author>Liu, Zhongdi ; Chen, Yifan ; Du, Zhe ; Zhu, Fengxue ; Huang, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-c52bd502411e00536bc152a2bc8f7f8ff585c3bae1c90fed706747fb552b25dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Acute Kidney Injury - etiology</topic><topic>Acute Kidney Injury - prevention & control</topic><topic>Animals</topic><topic>Autophagy</topic><topic>Beclin-1 - metabolism</topic><topic>Clinical Study</topic><topic>Cytokines</topic><topic>Epithelial cells</topic><topic>HMGB1</topic><topic>HMGB1 Protein</topic><topic>Inflammation</topic><topic>Ischemia</topic><topic>ischemic postconditioning</topic><topic>Ischemic Postconditioning - methods</topic><topic>kidney</topic><topic>Kidneys</topic><topic>Limb ischemia</topic><topic>Rapamycin</topic><topic>Rats</topic><topic>Renal function</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - complications</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Sirolimus - pharmacology</topic><topic>Transmission electron microscopy</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Zhongdi</creatorcontrib><creatorcontrib>Chen, Yifan</creatorcontrib><creatorcontrib>Du, Zhe</creatorcontrib><creatorcontrib>Zhu, Fengxue</creatorcontrib><creatorcontrib>Huang, Wei</creatorcontrib><collection>Taylor & Francis 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>Immunology Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Research Library</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Renal failure</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Zhongdi</au><au>Chen, Yifan</au><au>Du, Zhe</au><au>Zhu, Fengxue</au><au>Huang, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ischemic postconditioning protects against acute kidney injury after limb ischemia reperfusion by regulating HMGB1 release and autophagy</atitle><jtitle>Renal failure</jtitle><addtitle>Ren Fail</addtitle><date>2023-12</date><risdate>2023</risdate><volume>45</volume><issue>1</issue><spage>2189482</spage><epage>2189482</epage><pages>2189482-2189482</pages><issn>0886-022X</issn><eissn>1525-6049</eissn><abstract>Ischemic postconditioning (I-PostC) has a protective effect against acute kidney injury (AKI) induced by limb ischemia-reperfusion (LIR); however, the exact mechanism remains to be elucidated. Our study aims to investigate the potential involvement of high-mobility group box 1 protein (HMGB1) and autophagy in renoprotection generated by I-PostC. A rat model of LIR-induced AKI was established and rats were randomly assigned to five groups: (i) sham-operated control, (ii) I/R, (iii) I/R + I-PostC, (iv) I/R + I-PostC + rapamycin (autophagy activator), and (v) I/R + I-PostC + 3-methyladenine (autophagy inhibitor). Morphological changes in the kidneys were assessed by histology, and ultrastructural changes in renal tubular epithelial cells and glomerular podocytes were observed by transmission electron microscopy. The levels of kidney function parameters, serum inflammatory factors, and autophagy markers were detected. The results showed that the levels of HMGB1, Beclin1, LC3-II/LC3-I, and inflammatory cytokines (TNF-α and IL-6) were significantly higher in the I/R group compared to the sham control in serum and in renal tissues. I-PostC significantly reduced the levels of HMGB1, Beclin1, LC3-II/LC3-I, and inflammatory cytokines in renal tissues and improved renal function. Renal histopathology and ultrastructural observations indicated that I-PostC alleviated renal tissue injury. In addition, rapamycin (autophagy activator) treatment increased the levels of inflammatory cytokine expression levels and decreased renal function, reversed the protective effect of I-PostC against LIR-induced AKI. In conclusion, I-PostC could play a protective role against AKI by regulating the release of HMGB1 and inhibiting autophagy activation.</abstract><cop>England</cop><pub>Taylor & Francis</pub><pmid>37158301</pmid><doi>10.1080/0886022X.2023.2189482</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Kidney Injury - etiology Acute Kidney Injury - prevention & control Animals Autophagy Beclin-1 - metabolism Clinical Study Cytokines Epithelial cells HMGB1 HMGB1 Protein Inflammation Ischemia ischemic postconditioning Ischemic Postconditioning - methods kidney Kidneys Limb ischemia Rapamycin Rats Renal function Reperfusion Reperfusion Injury - complications Reperfusion Injury - prevention & control Sirolimus - pharmacology Transmission electron microscopy Tumor necrosis factor-α |
| title | Ischemic postconditioning protects against acute kidney injury after limb ischemia reperfusion by regulating HMGB1 release and autophagy |
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