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Bone marrow mesenchymal stem cells ameliorated kidney fibrosis by attenuating TLR4/NF-κB in diabetic rats
Diabetic nephropathy (DN) is a chronic inflammatory complication of diabetes mellitus, which becomes the most common cause of end-stage renal disease (ESRD). Recently, bone marrow mesenchymal stem cells (BMSCs) are considered as a promising therapy for DN. However, the protective mechanism of BMSCs...
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Published in: | Life sciences (1973) 2020-12, Vol.262, p.118385-8, Article 118385 |
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description | Diabetic nephropathy (DN) is a chronic inflammatory complication of diabetes mellitus, which becomes the most common cause of end-stage renal disease (ESRD). Recently, bone marrow mesenchymal stem cells (BMSCs) are considered as a promising therapy for DN. However, the protective mechanism of BMSCs on DN remains unclear. This study was done to explore the effect of a bone marrow stromal cell (BMSCs) transplant on DN rats and rat glomerular mesangial cells in high-glucose concentration. Diabetic rats were induced by a single intraperitoneal injection of streptozotocin (STZ) 65 mg/kg, then 4 × 106 BMSCs were transplanted in diabetic rats as the treatment group. Six weeks after BMSCs transplantation, blood serum creatinine (Scr) and blood urea nitrogen (BUN) were used to test renal function. Renal pathological examination was observed by HE staining, Masson staining, PAS staining and immunohistochemistry. The results demonstrated that BMSCs could dramatically improve renal function and collagen accumulation by reducing Scr, BUN, collagen I and IV expression and histopathological abnormalities in the diabetic kidneys. Furthermore, BMSCs could significantly attenuate the expression of TLR4/NF-κB and MCP-1 in vitro and in vivo (P |
doi_str_mv | 10.1016/j.lfs.2020.118385 |
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•BMSCs improved Scr and BUN levels in STZ-induced diabetic nephropathy rats.•BMSCs ameliorated renal injury and mesangial cells proliferation with hyperglycemia.•BMSCs reduced renal fibrosis by down-regulation of collagen accumulation.•BMSCs inhibited renal inflammation by suppression of TLR-4 NF-κB and MCP-1 in vivo and in vitro.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2020.118385</identifier><identifier>PMID: 32926926</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Abnormalities ; Animals ; Blood ; Blood Urea Nitrogen ; BMSCs ; Bone marrow ; Bone marrow transplantation ; Cells, Cultured ; Collagen ; Collagen (type I) ; Creatinine ; Creatinine - blood ; Cytokines ; Cytokines - metabolism ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - therapy ; Diabetic Nephropathies - prevention & control ; Diabetic nephropathy ; End-stage renal disease ; Female ; Fibrosis ; Glucose - metabolism ; Immunohistochemistry ; In vivo methods and tests ; Inflammation ; Kidney diseases ; Kidneys ; Mesangial cells ; Mesangial Cells - metabolism ; Mesenchymal Stem Cell Transplantation - methods ; Mesenchymal stem cells ; Monocyte chemoattractant protein 1 ; Nephropathy ; NF-kappa B - genetics ; NF-κB protein ; Rat ; Rats ; Rats, Sprague-Dawley ; Renal function ; Rodents ; Staining ; Stem cell transplantation ; Stem cells ; Streptozocin ; TLR4 protein ; TLR4/NF-κB ; Toll-Like Receptor 4 - genetics ; Toll-like receptors ; Transplantation ; Transplants & implants ; Urea</subject><ispartof>Life sciences (1973), 2020-12, Vol.262, p.118385-8, Article 118385</ispartof><rights>2020</rights><rights>Copyright © 2020. Published by Elsevier Inc.</rights><rights>Copyright Elsevier BV Dec 1, 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-6b876941a61fb99ab357b014f6a4345e10f8b581c054e42e48c8963f7eaccf873</citedby><cites>FETCH-LOGICAL-c381t-6b876941a61fb99ab357b014f6a4345e10f8b581c054e42e48c8963f7eaccf873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32926926$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Liya</creatorcontrib><creatorcontrib>Lin, Hefeng</creatorcontrib><creatorcontrib>Wang, Daijuanru</creatorcontrib><creatorcontrib>Bao, Zeying</creatorcontrib><creatorcontrib>Cai, Huabo</creatorcontrib><creatorcontrib>Zhang, Xiaoming</creatorcontrib><title>Bone marrow mesenchymal stem cells ameliorated kidney fibrosis by attenuating TLR4/NF-κB in diabetic rats</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Diabetic nephropathy (DN) is a chronic inflammatory complication of diabetes mellitus, which becomes the most common cause of end-stage renal disease (ESRD). Recently, bone marrow mesenchymal stem cells (BMSCs) are considered as a promising therapy for DN. However, the protective mechanism of BMSCs on DN remains unclear. This study was done to explore the effect of a bone marrow stromal cell (BMSCs) transplant on DN rats and rat glomerular mesangial cells in high-glucose concentration. Diabetic rats were induced by a single intraperitoneal injection of streptozotocin (STZ) 65 mg/kg, then 4 × 106 BMSCs were transplanted in diabetic rats as the treatment group. Six weeks after BMSCs transplantation, blood serum creatinine (Scr) and blood urea nitrogen (BUN) were used to test renal function. Renal pathological examination was observed by HE staining, Masson staining, PAS staining and immunohistochemistry. The results demonstrated that BMSCs could dramatically improve renal function and collagen accumulation by reducing Scr, BUN, collagen I and IV expression and histopathological abnormalities in the diabetic kidneys. Furthermore, BMSCs could significantly attenuate the expression of TLR4/NF-κB and MCP-1 in vitro and in vivo (P < 0.05, vs diabetic groups). This study reported a novel finding that BMSCs play a protective role in inhibition of inflammatory and fibrotic cytokines by down-regulating TLR-4/NF-κB expression under diabetic condition.
[Display omitted]
•BMSCs improved Scr and BUN levels in STZ-induced diabetic nephropathy rats.•BMSCs ameliorated renal injury and mesangial cells proliferation with hyperglycemia.•BMSCs reduced renal fibrosis by down-regulation of collagen accumulation.•BMSCs inhibited renal inflammation by suppression of TLR-4 NF-κB and MCP-1 in vivo and in vitro.</description><subject>Abnormalities</subject><subject>Animals</subject><subject>Blood</subject><subject>Blood Urea Nitrogen</subject><subject>BMSCs</subject><subject>Bone marrow</subject><subject>Bone marrow transplantation</subject><subject>Cells, Cultured</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Creatinine</subject><subject>Creatinine - blood</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - complications</subject><subject>Diabetes Mellitus, Experimental - therapy</subject><subject>Diabetic Nephropathies - prevention & control</subject><subject>Diabetic nephropathy</subject><subject>End-stage renal disease</subject><subject>Female</subject><subject>Fibrosis</subject><subject>Glucose - metabolism</subject><subject>Immunohistochemistry</subject><subject>In vivo methods and tests</subject><subject>Inflammation</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Mesangial cells</subject><subject>Mesangial Cells - metabolism</subject><subject>Mesenchymal Stem Cell Transplantation - methods</subject><subject>Mesenchymal stem cells</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Nephropathy</subject><subject>NF-kappa B - genetics</subject><subject>NF-κB protein</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renal function</subject><subject>Rodents</subject><subject>Staining</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Streptozocin</subject><subject>TLR4 protein</subject><subject>TLR4/NF-κB</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-like receptors</subject><subject>Transplantation</subject><subject>Transplants & implants</subject><subject>Urea</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp9kc2KFDEUhYMoTs_oA7iRgBs31ZP_SuHKGZxRaBRkXIckdaMp62dMUiP9aj6Ez2TaHl24EAKXwHcO956D0DNKtpRQdT5sx5C3jLD6p5pr-QBtqG67hihOH6INIUw0nBF5gk5zHgghUrb8MTrhrGOqvg0aLpYZ8GRTWr7jCTLM_st-siPOBSbsYRwzthOMcUm2QI-_xn6GPQ7RpSXHjN0e21JgXm2J82d8s_sozt9fNT9_XOA44z5aByV6XMX5CXoU7Jjh6f08Q5-u3txcvm12H67fXb7eNZ5rWhrldKs6Qa2iwXWddVy2jlARlBVcSKAkaCc19UQKEAyE9rpTPLRgvQ-65Wfo5dH3Ni3fVsjFTDEfLrEzLGs2TAimhdRCVfTFP-iwrGmu21VKd1pp8duQHilfb84JgrlNsUa2N5SYQxFmMLUIcyjCHIuomuf3zquboP-r-JN8BV4dAahR3EVIJvtY04c-JvDF9Ev8j_0voMaYjg</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Lin, Liya</creator><creator>Lin, Hefeng</creator><creator>Wang, Daijuanru</creator><creator>Bao, Zeying</creator><creator>Cai, Huabo</creator><creator>Zhang, Xiaoming</creator><general>Elsevier Inc</general><general>Elsevier BV</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20201201</creationdate><title>Bone marrow mesenchymal stem cells ameliorated kidney fibrosis by attenuating TLR4/NF-κB in diabetic rats</title><author>Lin, Liya ; Lin, Hefeng ; Wang, Daijuanru ; Bao, Zeying ; Cai, Huabo ; Zhang, Xiaoming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-6b876941a61fb99ab357b014f6a4345e10f8b581c054e42e48c8963f7eaccf873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Abnormalities</topic><topic>Animals</topic><topic>Blood</topic><topic>Blood Urea Nitrogen</topic><topic>BMSCs</topic><topic>Bone marrow</topic><topic>Bone marrow transplantation</topic><topic>Cells, Cultured</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Creatinine</topic><topic>Creatinine - blood</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - complications</topic><topic>Diabetes Mellitus, Experimental - therapy</topic><topic>Diabetic Nephropathies - prevention & control</topic><topic>Diabetic nephropathy</topic><topic>End-stage renal disease</topic><topic>Female</topic><topic>Fibrosis</topic><topic>Glucose - metabolism</topic><topic>Immunohistochemistry</topic><topic>In vivo methods and tests</topic><topic>Inflammation</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Mesangial cells</topic><topic>Mesangial Cells - metabolism</topic><topic>Mesenchymal Stem Cell Transplantation - methods</topic><topic>Mesenchymal stem cells</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Nephropathy</topic><topic>NF-kappa B - genetics</topic><topic>NF-κB protein</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renal function</topic><topic>Rodents</topic><topic>Staining</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Streptozocin</topic><topic>TLR4 protein</topic><topic>TLR4/NF-κB</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-like receptors</topic><topic>Transplantation</topic><topic>Transplants & implants</topic><topic>Urea</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Liya</creatorcontrib><creatorcontrib>Lin, Hefeng</creatorcontrib><creatorcontrib>Wang, Daijuanru</creatorcontrib><creatorcontrib>Bao, Zeying</creatorcontrib><creatorcontrib>Cai, Huabo</creatorcontrib><creatorcontrib>Zhang, Xiaoming</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Liya</au><au>Lin, Hefeng</au><au>Wang, Daijuanru</au><au>Bao, Zeying</au><au>Cai, Huabo</au><au>Zhang, Xiaoming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bone marrow mesenchymal stem cells ameliorated kidney fibrosis by attenuating TLR4/NF-κB in diabetic rats</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2020-12-01</date><risdate>2020</risdate><volume>262</volume><spage>118385</spage><epage>8</epage><pages>118385-8</pages><artnum>118385</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Diabetic nephropathy (DN) is a chronic inflammatory complication of diabetes mellitus, which becomes the most common cause of end-stage renal disease (ESRD). Recently, bone marrow mesenchymal stem cells (BMSCs) are considered as a promising therapy for DN. However, the protective mechanism of BMSCs on DN remains unclear. This study was done to explore the effect of a bone marrow stromal cell (BMSCs) transplant on DN rats and rat glomerular mesangial cells in high-glucose concentration. Diabetic rats were induced by a single intraperitoneal injection of streptozotocin (STZ) 65 mg/kg, then 4 × 106 BMSCs were transplanted in diabetic rats as the treatment group. Six weeks after BMSCs transplantation, blood serum creatinine (Scr) and blood urea nitrogen (BUN) were used to test renal function. Renal pathological examination was observed by HE staining, Masson staining, PAS staining and immunohistochemistry. The results demonstrated that BMSCs could dramatically improve renal function and collagen accumulation by reducing Scr, BUN, collagen I and IV expression and histopathological abnormalities in the diabetic kidneys. Furthermore, BMSCs could significantly attenuate the expression of TLR4/NF-κB and MCP-1 in vitro and in vivo (P < 0.05, vs diabetic groups). This study reported a novel finding that BMSCs play a protective role in inhibition of inflammatory and fibrotic cytokines by down-regulating TLR-4/NF-κB expression under diabetic condition.
[Display omitted]
•BMSCs improved Scr and BUN levels in STZ-induced diabetic nephropathy rats.•BMSCs ameliorated renal injury and mesangial cells proliferation with hyperglycemia.•BMSCs reduced renal fibrosis by down-regulation of collagen accumulation.•BMSCs inhibited renal inflammation by suppression of TLR-4 NF-κB and MCP-1 in vivo and in vitro.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>32926926</pmid><doi>10.1016/j.lfs.2020.118385</doi><tpages>8</tpages></addata></record> |
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subjects | Abnormalities Animals Blood Blood Urea Nitrogen BMSCs Bone marrow Bone marrow transplantation Cells, Cultured Collagen Collagen (type I) Creatinine Creatinine - blood Cytokines Cytokines - metabolism Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - therapy Diabetic Nephropathies - prevention & control Diabetic nephropathy End-stage renal disease Female Fibrosis Glucose - metabolism Immunohistochemistry In vivo methods and tests Inflammation Kidney diseases Kidneys Mesangial cells Mesangial Cells - metabolism Mesenchymal Stem Cell Transplantation - methods Mesenchymal stem cells Monocyte chemoattractant protein 1 Nephropathy NF-kappa B - genetics NF-κB protein Rat Rats Rats, Sprague-Dawley Renal function Rodents Staining Stem cell transplantation Stem cells Streptozocin TLR4 protein TLR4/NF-κB Toll-Like Receptor 4 - genetics Toll-like receptors Transplantation Transplants & implants Urea |
title | Bone marrow mesenchymal stem cells ameliorated kidney fibrosis by attenuating TLR4/NF-κB in diabetic rats |
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