Artesunate relieves acute kidney injury through inhibiting macrophagic Mincle‐mediated necroptosis and inflammation to tubular epithelial cell
Artesunate is a widely used derivative of artemisinin for malaria. Recent researches have shown that artesunate has a significant anti‐inflammatory effect on many diseases. However, its effect on acute kidney injury with a significant inflammatory response is not clear. In this study, we established...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2021-09, Vol.25 (18), p.8775-8788 |
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| creator | Lei, Xian‐ying Tan, Rui‐zhi Jia, Jian Wu, Song‐lin Wen, Cheng‐li Lin, Xiao Wang, Huan Shi, Zhang‐jing Li, Bo Kang, Yan Wang, Li |
| description | Artesunate is a widely used derivative of artemisinin for malaria. Recent researches have shown that artesunate has a significant anti‐inflammatory effect on many diseases. However, its effect on acute kidney injury with a significant inflammatory response is not clear. In this study, we established a cisplatin‐induced AKI mouse model and a co‐culture system of BMDM and tubular epithelial cells (mTEC) to verify the renoprotective and anti‐inflammatory effects of artesunate on AKI, and explored the underlying mechanism. We found that artesunate strongly down‐regulated the serum creatinine and BUN levels in AKI mice, reduced the necroptosis of tubular cells and down‐regulated the expression of the tubular injury molecule Tim‐1. On the other hand, artesunate strongly inhibited the mRNA expression of inflammatory cytokines (IL‐1β, IL‐6 and TNF‐α), protein levels of inflammatory signals (iNOS and NF‐κB) and necroptosis signals (RIPK1, RIPK3 and MLKL) in kidney of AKI mouse. Notably, the co‐culture system proved that Mincle in macrophage can aggravate the inflammation and necroptosis of mTEC induced by LPS, and artesunate suppressed the expression of Mincle in macrophage of kidney in AKI mouse. Overexpression of Mincle in BMDM restored the damage and necroptosis inhibited by artesunate in mTEC, indicating Mincle in macrophage is the target of artesunate to protect tubule cells in AKI. Our findings demonstrated that artesunate can significantly improve renal function in AKI, which may be related to the inhibition of Mincle‐mediated macrophage inflammation, thereby reducing the damage and necroptosis to tubular cells that provide new option for the treatment of AKI. |
| doi_str_mv | 10.1111/jcmm.16833 |
| format | Article |
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Recent researches have shown that artesunate has a significant anti‐inflammatory effect on many diseases. However, its effect on acute kidney injury with a significant inflammatory response is not clear. In this study, we established a cisplatin‐induced AKI mouse model and a co‐culture system of BMDM and tubular epithelial cells (mTEC) to verify the renoprotective and anti‐inflammatory effects of artesunate on AKI, and explored the underlying mechanism. We found that artesunate strongly down‐regulated the serum creatinine and BUN levels in AKI mice, reduced the necroptosis of tubular cells and down‐regulated the expression of the tubular injury molecule Tim‐1. On the other hand, artesunate strongly inhibited the mRNA expression of inflammatory cytokines (IL‐1β, IL‐6 and TNF‐α), protein levels of inflammatory signals (iNOS and NF‐κB) and necroptosis signals (RIPK1, RIPK3 and MLKL) in kidney of AKI mouse. Notably, the co‐culture system proved that Mincle in macrophage can aggravate the inflammation and necroptosis of mTEC induced by LPS, and artesunate suppressed the expression of Mincle in macrophage of kidney in AKI mouse. Overexpression of Mincle in BMDM restored the damage and necroptosis inhibited by artesunate in mTEC, indicating Mincle in macrophage is the target of artesunate to protect tubule cells in AKI. Our findings demonstrated that artesunate can significantly improve renal function in AKI, which may be related to the inhibition of Mincle‐mediated macrophage inflammation, thereby reducing the damage and necroptosis to tubular cells that provide new option for the treatment of AKI.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.16833</identifier><identifier>PMID: 34337860</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Acute Kidney Injury - drug therapy ; AKI ; Animals ; Anti-Inflammatory Agents - pharmacology ; Antibodies ; Artemisinin ; Artesunate ; Artesunate - pharmacology ; Cell culture ; Cisplatin ; Creatinine ; Epithelial cells ; Experiments ; Gene expression ; Inflammation ; Inflammation - drug therapy ; Kidneys ; Lipopolysaccharides ; Macrophages ; Malaria ; Male ; Mice ; Mice, Inbred C57BL ; Mincle ; Necroptosis ; Necroptosis - drug effects ; Nitric-oxide synthase ; Original ; Oxidative stress ; Primary Cell Culture ; Renal function ; Streptococcus infections ; Tumor necrosis factor</subject><ispartof>Journal of cellular and molecular medicine, 2021-09, Vol.25 (18), p.8775-8788</ispartof><rights>2021 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2021. This work is published under 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4483-a7c4e58333117ed9d0e15c3c09306dcd77487011ce8675389575f3bc19d3f02d3</citedby><cites>FETCH-LOGICAL-c4483-a7c4e58333117ed9d0e15c3c09306dcd77487011ce8675389575f3bc19d3f02d3</cites><orcidid>0000-0003-3881-3149</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/PMC8435453/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8435453/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34337860$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lei, Xian‐ying</creatorcontrib><creatorcontrib>Tan, Rui‐zhi</creatorcontrib><creatorcontrib>Jia, Jian</creatorcontrib><creatorcontrib>Wu, Song‐lin</creatorcontrib><creatorcontrib>Wen, Cheng‐li</creatorcontrib><creatorcontrib>Lin, Xiao</creatorcontrib><creatorcontrib>Wang, Huan</creatorcontrib><creatorcontrib>Shi, Zhang‐jing</creatorcontrib><creatorcontrib>Li, Bo</creatorcontrib><creatorcontrib>Kang, Yan</creatorcontrib><creatorcontrib>Wang, Li</creatorcontrib><title>Artesunate relieves acute kidney injury through inhibiting macrophagic Mincle‐mediated necroptosis and inflammation to tubular epithelial cell</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Artesunate is a widely used derivative of artemisinin for malaria. Recent researches have shown that artesunate has a significant anti‐inflammatory effect on many diseases. However, its effect on acute kidney injury with a significant inflammatory response is not clear. In this study, we established a cisplatin‐induced AKI mouse model and a co‐culture system of BMDM and tubular epithelial cells (mTEC) to verify the renoprotective and anti‐inflammatory effects of artesunate on AKI, and explored the underlying mechanism. We found that artesunate strongly down‐regulated the serum creatinine and BUN levels in AKI mice, reduced the necroptosis of tubular cells and down‐regulated the expression of the tubular injury molecule Tim‐1. On the other hand, artesunate strongly inhibited the mRNA expression of inflammatory cytokines (IL‐1β, IL‐6 and TNF‐α), protein levels of inflammatory signals (iNOS and NF‐κB) and necroptosis signals (RIPK1, RIPK3 and MLKL) in kidney of AKI mouse. Notably, the co‐culture system proved that Mincle in macrophage can aggravate the inflammation and necroptosis of mTEC induced by LPS, and artesunate suppressed the expression of Mincle in macrophage of kidney in AKI mouse. Overexpression of Mincle in BMDM restored the damage and necroptosis inhibited by artesunate in mTEC, indicating Mincle in macrophage is the target of artesunate to protect tubule cells in AKI. Our findings demonstrated that artesunate can significantly improve renal function in AKI, which may be related to the inhibition of Mincle‐mediated macrophage inflammation, thereby reducing the damage and necroptosis to tubular cells that provide new option for the treatment of AKI.</description><subject>Acute Kidney Injury - drug therapy</subject><subject>AKI</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antibodies</subject><subject>Artemisinin</subject><subject>Artesunate</subject><subject>Artesunate - pharmacology</subject><subject>Cell culture</subject><subject>Cisplatin</subject><subject>Creatinine</subject><subject>Epithelial cells</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Kidneys</subject><subject>Lipopolysaccharides</subject><subject>Macrophages</subject><subject>Malaria</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mincle</subject><subject>Necroptosis</subject><subject>Necroptosis - drug effects</subject><subject>Nitric-oxide synthase</subject><subject>Original</subject><subject>Oxidative stress</subject><subject>Primary Cell Culture</subject><subject>Renal function</subject><subject>Streptococcus infections</subject><subject>Tumor necrosis factor</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><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>eNp9kcFuEzEQhlcIREvhwgMgS1wqpBR7ba-9F6QqghbUiAucLceeZB28drC9RbnxCH1GngSHhAo44Mt4NJ__mfHfNM8JviD1vN6YcbwgnaT0QXNKuGxnrKfs4fFOJJUnzZOcNxjTjtD-cXNCGaVCdvi0ubtMBfIUdAGUwDu4hYy0mWr6xdkAO-TCZko7VIYUp_VQ08EtXXFhjUZtUtwOeu0MWrhgPPz4fjeCdVXMogD7aonZVcFg68OV1-Ooi4sBlYjKtJy8Tgi2rgy1s_bIgPdPm0cr7TM8O8az5vO7t5_m17Obj1fv55c3M8OYpDMtDANeV6aECLC9xUC4oQb3FHfWWCGYFJgQA7ITnMqeC76iS0N6S1e4tfSseXPQ3U7LOrOBUJL2apvcqNNORe3U35XgBrWOt0oyyhmnVeD8KJDi1wlyUaPL-w10gDhl1fLaklEs2oq-_AfdxCmFul6lBBG87Tiu1KsDVf8t5wSr-2EIVnuj1d5o9cvoCr_4c_x79LezFSAH4JvzsPuPlPowXywOoj8BPrS4Ug</recordid><startdate>202109</startdate><enddate>202109</enddate><creator>Lei, Xian‐ying</creator><creator>Tan, Rui‐zhi</creator><creator>Jia, Jian</creator><creator>Wu, Song‐lin</creator><creator>Wen, Cheng‐li</creator><creator>Lin, Xiao</creator><creator>Wang, Huan</creator><creator>Shi, Zhang‐jing</creator><creator>Li, Bo</creator><creator>Kang, Yan</creator><creator>Wang, Li</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</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>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3881-3149</orcidid></search><sort><creationdate>202109</creationdate><title>Artesunate relieves acute kidney injury through inhibiting macrophagic Mincle‐mediated necroptosis and inflammation to tubular epithelial cell</title><author>Lei, Xian‐ying ; Tan, Rui‐zhi ; Jia, Jian ; Wu, Song‐lin ; Wen, Cheng‐li ; Lin, Xiao ; Wang, Huan ; Shi, Zhang‐jing ; Li, Bo ; Kang, Yan ; Wang, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4483-a7c4e58333117ed9d0e15c3c09306dcd77487011ce8675389575f3bc19d3f02d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acute Kidney Injury - drug therapy</topic><topic>AKI</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Antibodies</topic><topic>Artemisinin</topic><topic>Artesunate</topic><topic>Artesunate - pharmacology</topic><topic>Cell culture</topic><topic>Cisplatin</topic><topic>Creatinine</topic><topic>Epithelial cells</topic><topic>Experiments</topic><topic>Gene expression</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Kidneys</topic><topic>Lipopolysaccharides</topic><topic>Macrophages</topic><topic>Malaria</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mincle</topic><topic>Necroptosis</topic><topic>Necroptosis - drug effects</topic><topic>Nitric-oxide synthase</topic><topic>Original</topic><topic>Oxidative stress</topic><topic>Primary Cell Culture</topic><topic>Renal function</topic><topic>Streptococcus infections</topic><topic>Tumor necrosis factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lei, Xian‐ying</creatorcontrib><creatorcontrib>Tan, Rui‐zhi</creatorcontrib><creatorcontrib>Jia, Jian</creatorcontrib><creatorcontrib>Wu, Song‐lin</creatorcontrib><creatorcontrib>Wen, Cheng‐li</creatorcontrib><creatorcontrib>Lin, Xiao</creatorcontrib><creatorcontrib>Wang, Huan</creatorcontrib><creatorcontrib>Shi, Zhang‐jing</creatorcontrib><creatorcontrib>Li, Bo</creatorcontrib><creatorcontrib>Kang, Yan</creatorcontrib><creatorcontrib>Wang, Li</creatorcontrib><collection>Wiley_OA刊</collection><collection>Wiley Online Library Journals</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</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>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 (ProQuest)</collection><collection>ProQuest Biological Science Journals</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lei, Xian‐ying</au><au>Tan, Rui‐zhi</au><au>Jia, Jian</au><au>Wu, Song‐lin</au><au>Wen, Cheng‐li</au><au>Lin, Xiao</au><au>Wang, Huan</au><au>Shi, Zhang‐jing</au><au>Li, Bo</au><au>Kang, Yan</au><au>Wang, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Artesunate relieves acute kidney injury through inhibiting macrophagic Mincle‐mediated necroptosis and inflammation to tubular epithelial cell</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2021-09</date><risdate>2021</risdate><volume>25</volume><issue>18</issue><spage>8775</spage><epage>8788</epage><pages>8775-8788</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Artesunate is a widely used derivative of artemisinin for malaria. Recent researches have shown that artesunate has a significant anti‐inflammatory effect on many diseases. However, its effect on acute kidney injury with a significant inflammatory response is not clear. In this study, we established a cisplatin‐induced AKI mouse model and a co‐culture system of BMDM and tubular epithelial cells (mTEC) to verify the renoprotective and anti‐inflammatory effects of artesunate on AKI, and explored the underlying mechanism. We found that artesunate strongly down‐regulated the serum creatinine and BUN levels in AKI mice, reduced the necroptosis of tubular cells and down‐regulated the expression of the tubular injury molecule Tim‐1. On the other hand, artesunate strongly inhibited the mRNA expression of inflammatory cytokines (IL‐1β, IL‐6 and TNF‐α), protein levels of inflammatory signals (iNOS and NF‐κB) and necroptosis signals (RIPK1, RIPK3 and MLKL) in kidney of AKI mouse. Notably, the co‐culture system proved that Mincle in macrophage can aggravate the inflammation and necroptosis of mTEC induced by LPS, and artesunate suppressed the expression of Mincle in macrophage of kidney in AKI mouse. Overexpression of Mincle in BMDM restored the damage and necroptosis inhibited by artesunate in mTEC, indicating Mincle in macrophage is the target of artesunate to protect tubule cells in AKI. Our findings demonstrated that artesunate can significantly improve renal function in AKI, which may be related to the inhibition of Mincle‐mediated macrophage inflammation, thereby reducing the damage and necroptosis to tubular cells that provide new option for the treatment of AKI.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>34337860</pmid><doi>10.1111/jcmm.16833</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0003-3881-3149</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Wiley_OA刊; Wiley Online Library (Online service); PubMed Central; EZB Electronic Journals Library |
| subjects | Acute Kidney Injury - drug therapy AKI Animals Anti-Inflammatory Agents - pharmacology Antibodies Artemisinin Artesunate Artesunate - pharmacology Cell culture Cisplatin Creatinine Epithelial cells Experiments Gene expression Inflammation Inflammation - drug therapy Kidneys Lipopolysaccharides Macrophages Malaria Male Mice Mice, Inbred C57BL Mincle Necroptosis Necroptosis - drug effects Nitric-oxide synthase Original Oxidative stress Primary Cell Culture Renal function Streptococcus infections Tumor necrosis factor |
| title | Artesunate relieves acute kidney injury through inhibiting macrophagic Mincle‐mediated necroptosis and inflammation to tubular epithelial cell |
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