Dexamethasone inhibited angiotensin II and its receptors to reduce sepsis-induced lung and kidney injury in rats
To investigate the effect of dexamethasone (DXM) on acute lung and kidney injury with sepsis and its possible mechanism. Control (NC), lipopolysaccharide (LPS) and lipopolysaccharide + dexamethasone (LPS+DXM) treated groups were established by random assignment of 72 Wistar rats. The NC rats were in...
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| description | To investigate the effect of dexamethasone (DXM) on acute lung and kidney injury with sepsis and its possible mechanism.
Control (NC), lipopolysaccharide (LPS) and lipopolysaccharide + dexamethasone (LPS+DXM) treated groups were established by random assignment of 72 Wistar rats. The NC rats were injected with physiological saline, while the LPS group was injected with LPS (5 mg/kg) and LPS+DXM group was injected with LPS(5 mg/kg) first and followed by DXM (1 mg/kg). Serum tumor necrosis factor-α (TNF-α) and serum macrophage inflammatory protein 1α (MIP-1α) were measured by ELISA. Lung wet/dry weight ratio, serum creatinine(SCR) and blood urea nitrogen(BUN) were determined at various time points. Hematoxylin Eosin staining (HE) for pathological changes in the lung and kidney. Radioimmunoassay was used to detect the levels of angiotensin II (Ang II) in plasma, lung and kidney tissues. Immunohistochemistry and western blot (WB) were used to detect angiotensin II receptor type 1 (AT1R) protein and angiotensin II receptor type 2 (AT2R) protein in lung and kidney tissues. The level of nitric oxide (NO) in serum, lung and kidney were detected using nitrate reductase method.
Compared with control group, serum TNF-α, MIP-1α, SCR, BUN, lung W/D, Ang II level in plasma, lung and kidney, lung and kidney AT2R protein, NO level in serum, lung and kidney were significantly elevated(P |
| doi_str_mv | 10.1371/journal.pone.0308557 |
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Control (NC), lipopolysaccharide (LPS) and lipopolysaccharide + dexamethasone (LPS+DXM) treated groups were established by random assignment of 72 Wistar rats. The NC rats were injected with physiological saline, while the LPS group was injected with LPS (5 mg/kg) and LPS+DXM group was injected with LPS(5 mg/kg) first and followed by DXM (1 mg/kg). Serum tumor necrosis factor-α (TNF-α) and serum macrophage inflammatory protein 1α (MIP-1α) were measured by ELISA. Lung wet/dry weight ratio, serum creatinine(SCR) and blood urea nitrogen(BUN) were determined at various time points. Hematoxylin Eosin staining (HE) for pathological changes in the lung and kidney. Radioimmunoassay was used to detect the levels of angiotensin II (Ang II) in plasma, lung and kidney tissues. Immunohistochemistry and western blot (WB) were used to detect angiotensin II receptor type 1 (AT1R) protein and angiotensin II receptor type 2 (AT2R) protein in lung and kidney tissues. The level of nitric oxide (NO) in serum, lung and kidney were detected using nitrate reductase method.
Compared with control group, serum TNF-α, MIP-1α, SCR, BUN, lung W/D, Ang II level in plasma, lung and kidney, lung and kidney AT2R protein, NO level in serum, lung and kidney were significantly elevated(P<0.05) and pathological damage of lung and kidney tissues were showed in LPS group rats (P<0.05), whereas DXM down-regulated the above indexes and alleviate pathological damage of lung and kidney tissues. However, the expression of the lung and kidney AT1R protein was opposite to the above results.
Sepsis can cause acute lung and kidney injury and changes RAAS components in circulating, lung and renal. DXM can improve acute lung and kidney injury in septic rats, and the mechanism may be related to the down-regulation of inflammatory factors, AngII, AT2R, NO and up-regulation of AT1R expression by DXM.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0308557</identifier><identifier>PMID: 39178201</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acute Kidney Injury - drug therapy ; Acute Kidney Injury - etiology ; Acute Kidney Injury - metabolism ; Acute Kidney Injury - pathology ; Acute Kidney Injury - prevention & control ; Acute Lung Injury - drug therapy ; Acute Lung Injury - etiology ; Acute Lung Injury - metabolism ; Acute Lung Injury - pathology ; Acute Lung Injury - prevention & control ; Angiotensin ; Angiotensin AT1 receptors ; Angiotensin AT2 receptors ; Angiotensin II ; Animals ; Antibodies ; Biochemistry ; Biology ; Biotechnology ; Blood Urea Nitrogen ; Complications and side effects ; Creatinine ; Damage ; Dexamethasone ; Dexamethasone - pharmacology ; Down-regulation ; Drug therapy ; Enzyme-linked immunosorbent assay ; Experiments ; Immunohistochemistry ; Inflammation ; Injuries ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; Kidney failure ; Kidneys ; Lipopolysaccharides ; Lung - drug effects ; Lung - metabolism ; Lung - pathology ; Lung diseases ; Lungs ; Macrophage inflammatory protein ; Male ; Nitrate reductase ; Nitric oxide ; Nitric Oxide - metabolism ; Physiological effects ; Plasma ; Protein expression ; Proteins ; Radioimmunoassay ; Rats ; Rats, Wistar ; Receptor, Angiotensin, Type 1 - metabolism ; Receptor, Angiotensin, Type 2 - metabolism ; Receptors ; Reductases ; Sepsis ; Sepsis - complications ; Sepsis - drug therapy ; Sepsis - metabolism ; Testing ; Tumor Necrosis Factor-alpha - blood ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-α ; Urea</subject><ispartof>PloS one, 2024-08, Vol.19 (8), p.e0308557</ispartof><rights>Copyright: © 2024 Zhan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>COPYRIGHT 2024 Public Library of Science</rights><rights>2024 Zhan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024 Zhan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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><orcidid>0000-0003-1109-1502 ; 0000-0002-8409-6163</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0308557&type=printable$$EPDF$$P50$$Gplos$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0308557$$EHTML$$P50$$Gplos$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,864,2102,23866,27924,27925,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39178201$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhan, Zhuqin</creatorcontrib><creatorcontrib>Lian, Zhulan</creatorcontrib><creatorcontrib>Bai, Haitao</creatorcontrib><title>Dexamethasone inhibited angiotensin II and its receptors to reduce sepsis-induced lung and kidney injury in rats</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>To investigate the effect of dexamethasone (DXM) on acute lung and kidney injury with sepsis and its possible mechanism.
Control (NC), lipopolysaccharide (LPS) and lipopolysaccharide + dexamethasone (LPS+DXM) treated groups were established by random assignment of 72 Wistar rats. The NC rats were injected with physiological saline, while the LPS group was injected with LPS (5 mg/kg) and LPS+DXM group was injected with LPS(5 mg/kg) first and followed by DXM (1 mg/kg). Serum tumor necrosis factor-α (TNF-α) and serum macrophage inflammatory protein 1α (MIP-1α) were measured by ELISA. Lung wet/dry weight ratio, serum creatinine(SCR) and blood urea nitrogen(BUN) were determined at various time points. Hematoxylin Eosin staining (HE) for pathological changes in the lung and kidney. Radioimmunoassay was used to detect the levels of angiotensin II (Ang II) in plasma, lung and kidney tissues. Immunohistochemistry and western blot (WB) were used to detect angiotensin II receptor type 1 (AT1R) protein and angiotensin II receptor type 2 (AT2R) protein in lung and kidney tissues. The level of nitric oxide (NO) in serum, lung and kidney were detected using nitrate reductase method.
Compared with control group, serum TNF-α, MIP-1α, SCR, BUN, lung W/D, Ang II level in plasma, lung and kidney, lung and kidney AT2R protein, NO level in serum, lung and kidney were significantly elevated(P<0.05) and pathological damage of lung and kidney tissues were showed in LPS group rats (P<0.05), whereas DXM down-regulated the above indexes and alleviate pathological damage of lung and kidney tissues. However, the expression of the lung and kidney AT1R protein was opposite to the above results.
Sepsis can cause acute lung and kidney injury and changes RAAS components in circulating, lung and renal. DXM can improve acute lung and kidney injury in septic rats, and the mechanism may be related to the down-regulation of inflammatory factors, AngII, AT2R, NO and up-regulation of AT1R expression by DXM.</description><subject>Acute Kidney Injury - drug therapy</subject><subject>Acute Kidney Injury - etiology</subject><subject>Acute Kidney Injury - metabolism</subject><subject>Acute Kidney Injury - pathology</subject><subject>Acute Kidney Injury - prevention & control</subject><subject>Acute Lung Injury - drug therapy</subject><subject>Acute Lung Injury - etiology</subject><subject>Acute Lung Injury - metabolism</subject><subject>Acute Lung Injury - pathology</subject><subject>Acute Lung Injury - prevention & control</subject><subject>Angiotensin</subject><subject>Angiotensin AT1 receptors</subject><subject>Angiotensin AT2 receptors</subject><subject>Angiotensin II</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Biochemistry</subject><subject>Biology</subject><subject>Biotechnology</subject><subject>Blood Urea Nitrogen</subject><subject>Complications and side effects</subject><subject>Creatinine</subject><subject>Damage</subject><subject>Dexamethasone</subject><subject>Dexamethasone - pharmacology</subject><subject>Down-regulation</subject><subject>Drug therapy</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Experiments</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney failure</subject><subject>Kidneys</subject><subject>Lipopolysaccharides</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lung diseases</subject><subject>Lungs</subject><subject>Macrophage inflammatory protein</subject><subject>Male</subject><subject>Nitrate reductase</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Physiological effects</subject><subject>Plasma</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Radioimmunoassay</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>Receptor, Angiotensin, Type 2 - metabolism</subject><subject>Receptors</subject><subject>Reductases</subject><subject>Sepsis</subject><subject>Sepsis - complications</subject><subject>Sepsis - drug therapy</subject><subject>Sepsis - metabolism</subject><subject>Testing</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-α</subject><subject>Urea</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkttq3DAQhk1paQ7tG5TWUCjthbc6WLJ8GdLTQiDQ062RpdGutrbkSjIkbx9t4pZsyUXRxegfvvlHGqkoXmC0wrTB73d-Dk4Oq8k7WCGKBGPNo-IYt5RUnCD6-N7-qDiJcYcQo4Lzp8URbXEjCMLHxfQBruQIaStj9imt29reJtCldBvrE7hoXbleZ6lLm2IZQMGUfIhl8lnoWUEZYYo2VtbtlS6H2W1u-V9WO7jOnrs57EMZZIrPiidGDhGeL_G0-PHp4_fzL9XF5ef1-dlFpesGp6rGCBoOQtR9y0iNqGqBS2G46ImplUKMa9UrEDUB3hAjsRRCMWaIxJiyhp4Wr-58p8HHbhlW7ChqOaMNYzwT6ztCe7nrpmBHGa47L213m_Bh08mQrBqgE9QYrWojayzqGvIUERE9boxShDDTZq-3S7fgf88QUzfaqGAYpAM_L22ZaLnI6Ot_0IcPt1AbmftbZ3wKUu1NuzOBmGhI2-69Vg9QeWkYrcoPamzOHxS8OyjITIKrtJFzjN3629f_Zy9_HrJv7rFbkEPaRj_MyXoXD8GXy-3nfgT9d-x_fiS9AYfP4Bw</recordid><startdate>20240823</startdate><enddate>20240823</enddate><creator>Zhan, Zhuqin</creator><creator>Lian, Zhulan</creator><creator>Bai, Haitao</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-1109-1502</orcidid><orcidid>https://orcid.org/0000-0002-8409-6163</orcidid></search><sort><creationdate>20240823</creationdate><title>Dexamethasone inhibited angiotensin II and its receptors to reduce sepsis-induced lung and kidney injury in rats</title><author>Zhan, Zhuqin ; Lian, Zhulan ; Bai, Haitao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-d471t-410e76e884b952403c9e6a8f68b2f4cc056dcbce842e672fa1a88c55f2a113573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acute Kidney Injury - drug therapy</topic><topic>Acute Kidney Injury - etiology</topic><topic>Acute Kidney Injury - metabolism</topic><topic>Acute Kidney Injury - pathology</topic><topic>Acute Kidney Injury - prevention & control</topic><topic>Acute Lung Injury - drug therapy</topic><topic>Acute Lung Injury - etiology</topic><topic>Acute Lung Injury - metabolism</topic><topic>Acute Lung Injury - pathology</topic><topic>Acute Lung Injury - prevention & control</topic><topic>Angiotensin</topic><topic>Angiotensin AT1 receptors</topic><topic>Angiotensin AT2 receptors</topic><topic>Angiotensin II</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Biochemistry</topic><topic>Biology</topic><topic>Biotechnology</topic><topic>Blood Urea Nitrogen</topic><topic>Complications and side effects</topic><topic>Creatinine</topic><topic>Damage</topic><topic>Dexamethasone</topic><topic>Dexamethasone - pharmacology</topic><topic>Down-regulation</topic><topic>Drug therapy</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Experiments</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Injuries</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney failure</topic><topic>Kidneys</topic><topic>Lipopolysaccharides</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lung diseases</topic><topic>Lungs</topic><topic>Macrophage inflammatory protein</topic><topic>Male</topic><topic>Nitrate reductase</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Physiological effects</topic><topic>Plasma</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Radioimmunoassay</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>Receptor, Angiotensin, Type 2 - metabolism</topic><topic>Receptors</topic><topic>Reductases</topic><topic>Sepsis</topic><topic>Sepsis - complications</topic><topic>Sepsis - drug therapy</topic><topic>Sepsis - metabolism</topic><topic>Testing</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-α</topic><topic>Urea</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhan, Zhuqin</creatorcontrib><creatorcontrib>Lian, Zhulan</creatorcontrib><creatorcontrib>Bai, Haitao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science 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>ProQuest Materials Science Collection</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 & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhan, Zhuqin</au><au>Lian, Zhulan</au><au>Bai, Haitao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dexamethasone inhibited angiotensin II and its receptors to reduce sepsis-induced lung and kidney injury in rats</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2024-08-23</date><risdate>2024</risdate><volume>19</volume><issue>8</issue><spage>e0308557</spage><pages>e0308557-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>To investigate the effect of dexamethasone (DXM) on acute lung and kidney injury with sepsis and its possible mechanism.
Control (NC), lipopolysaccharide (LPS) and lipopolysaccharide + dexamethasone (LPS+DXM) treated groups were established by random assignment of 72 Wistar rats. The NC rats were injected with physiological saline, while the LPS group was injected with LPS (5 mg/kg) and LPS+DXM group was injected with LPS(5 mg/kg) first and followed by DXM (1 mg/kg). Serum tumor necrosis factor-α (TNF-α) and serum macrophage inflammatory protein 1α (MIP-1α) were measured by ELISA. Lung wet/dry weight ratio, serum creatinine(SCR) and blood urea nitrogen(BUN) were determined at various time points. Hematoxylin Eosin staining (HE) for pathological changes in the lung and kidney. Radioimmunoassay was used to detect the levels of angiotensin II (Ang II) in plasma, lung and kidney tissues. Immunohistochemistry and western blot (WB) were used to detect angiotensin II receptor type 1 (AT1R) protein and angiotensin II receptor type 2 (AT2R) protein in lung and kidney tissues. The level of nitric oxide (NO) in serum, lung and kidney were detected using nitrate reductase method.
Compared with control group, serum TNF-α, MIP-1α, SCR, BUN, lung W/D, Ang II level in plasma, lung and kidney, lung and kidney AT2R protein, NO level in serum, lung and kidney were significantly elevated(P<0.05) and pathological damage of lung and kidney tissues were showed in LPS group rats (P<0.05), whereas DXM down-regulated the above indexes and alleviate pathological damage of lung and kidney tissues. However, the expression of the lung and kidney AT1R protein was opposite to the above results.
Sepsis can cause acute lung and kidney injury and changes RAAS components in circulating, lung and renal. DXM can improve acute lung and kidney injury in septic rats, and the mechanism may be related to the down-regulation of inflammatory factors, AngII, AT2R, NO and up-regulation of AT1R expression by DXM.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>39178201</pmid><doi>10.1371/journal.pone.0308557</doi><tpages>e0308557</tpages><orcidid>https://orcid.org/0000-0003-1109-1502</orcidid><orcidid>https://orcid.org/0000-0002-8409-6163</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2024-08, Vol.19 (8), p.e0308557 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_3096537556 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Acute Kidney Injury - drug therapy Acute Kidney Injury - etiology Acute Kidney Injury - metabolism Acute Kidney Injury - pathology Acute Kidney Injury - prevention & control Acute Lung Injury - drug therapy Acute Lung Injury - etiology Acute Lung Injury - metabolism Acute Lung Injury - pathology Acute Lung Injury - prevention & control Angiotensin Angiotensin AT1 receptors Angiotensin AT2 receptors Angiotensin II Animals Antibodies Biochemistry Biology Biotechnology Blood Urea Nitrogen Complications and side effects Creatinine Damage Dexamethasone Dexamethasone - pharmacology Down-regulation Drug therapy Enzyme-linked immunosorbent assay Experiments Immunohistochemistry Inflammation Injuries Kidney - drug effects Kidney - metabolism Kidney - pathology Kidney failure Kidneys Lipopolysaccharides Lung - drug effects Lung - metabolism Lung - pathology Lung diseases Lungs Macrophage inflammatory protein Male Nitrate reductase Nitric oxide Nitric Oxide - metabolism Physiological effects Plasma Protein expression Proteins Radioimmunoassay Rats Rats, Wistar Receptor, Angiotensin, Type 1 - metabolism Receptor, Angiotensin, Type 2 - metabolism Receptors Reductases Sepsis Sepsis - complications Sepsis - drug therapy Sepsis - metabolism Testing Tumor Necrosis Factor-alpha - blood Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α Urea |
| title | Dexamethasone inhibited angiotensin II and its receptors to reduce sepsis-induced lung and kidney injury in rats |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-05T00%3A53%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Dexamethasone%20inhibited%20angiotensin%20II%20and%20its%20receptors%20to%20reduce%20sepsis-induced%20lung%20and%20kidney%20injury%20in%20rats&rft.jtitle=PloS%20one&rft.au=Zhan,%20Zhuqin&rft.date=2024-08-23&rft.volume=19&rft.issue=8&rft.spage=e0308557&rft.pages=e0308557-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0308557&rft_dat=%3Cgale_plos_%3EA805872998%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3096537556&rft_id=info:pmid/39178201&rft_galeid=A805872998&rft_doaj_id=oai_doaj_org_article_83ffdc4fa41844e386028b17fcc225f9&rfr_iscdi=true |