Xanthenone, ACE2 activator, counteracted gentamicin-induced nephrotoxicity in rats: Impact on oxidative stress and ACE2/Ang-(1–7) signaling
Nephrotoxicity is a rapid deterioration of kidney function due to exposure to nephrotoxic drugs as gentamicin. Gentamicin increases the generation of reactive oxygen species (ROS) leading to inflammatory responses and nuclear factor-κB (NF-κB) activation. The renal renin-angiotensin system (RAS) is...
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| creator | Abdel-Fattah, Maha M. Elgendy, Abdel Nasser.A.M. Mohamed, Wafaa R. |
| description | Nephrotoxicity is a rapid deterioration of kidney function due to exposure to nephrotoxic drugs as gentamicin. Gentamicin increases the generation of reactive oxygen species (ROS) leading to inflammatory responses and nuclear factor-κB (NF-κB) activation. The renal renin-angiotensin system (RAS) is considered a crucial regulator for physiological homeostasis and disease progression through the classic ACE/Ang-II/AT1 axis and its antagonist, ACE2/Ang-(1–7)/Mas axis which exerts an important role in the kidney. The present study evaluates the protective effects of the angiotensin-converting enzyme 2 (ACE2) activator; xanthenone; against experimental nephrotoxicity induced by gentamicin. Rats were divided into 4 groups, normal control, xanthenone (2 mg/kg, s.c), gentamicin (100 mg/kg, i.p. for one week) and xanthenone + gentamicin groups. Blood urea nitrogen (BUN) and serum creatinine levels were measured. The kidney tissues were used for estimating glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), NF-κB, Angiotensin II (AngII), and Ang-(1–7). In addition, histopathological examination and Western blot analysis of ACE2 expression were done. Xanthenone significantly restored serum levels of BUN and creatinine. Xanthenone exerted significant antioxidant effect as revealed by increased GSH content and SOD activity together with reduced MDA content. It exerted anti-inflammatory effect by significant reduction in TNF-α, NF-κB and IL-6 expression compared to gentamicin group. Xanthenone increased Ang-(1–7) and ACE2 expression while significantly decreased Ang-II expression. Histopathologically, xanthenone markedly counteracted gentamicin-induced renal aberrations. Activation of ACE2/Ang-(1–7) by xanthenone produced significant antioxidant and anti-inflammatory effects that counteracted gentamicin-induced nephrotoxicity.
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| doi_str_mv | 10.1016/j.lfs.2021.119387 |
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[Display omitted]</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2021.119387</identifier><identifier>PMID: 33774027</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>ACE2 ; ACE2 activator ; Acute Kidney Injury - chemically induced ; Acute Kidney Injury - prevention & control ; Ang-(1–7) ; Angiotensin ; Angiotensin I - metabolism ; Angiotensin II ; Angiotensin-converting enzyme 2 ; Angiotensin-Converting Enzyme 2 - drug effects ; Angiotensin-Converting Enzyme 2 - metabolism ; Animals ; Antioxidants ; Blotting, Western ; Creatinine ; Gentamicin ; Gentamicins - toxicity ; Glutathione ; Homeostasis ; Inflammation ; Interleukin 6 ; Interleukins - metabolism ; Kidneys ; Male ; Malondialdehyde ; Nephrotoxicity ; NF-κB protein ; Oxidative stress ; Oxidative Stress - drug effects ; Peptide Fragments - metabolism ; Peptidyl-dipeptidase A ; Rats ; Rats, Wistar ; Reactive oxygen species ; Renin ; Serum levels ; Signal Transduction - drug effects ; Superoxide dismutase ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Urea ; Xanthenone ; Xanthones - pharmacology</subject><ispartof>Life sciences (1973), 2021-06, Vol.275, p.119387, Article 119387</ispartof><rights>2021</rights><rights>Copyright © 2021. Published by Elsevier Inc.</rights><rights>Copyright Elsevier BV Jun 15, 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-a2ba7a7ec7170103f346423ace93f8bbb97d6db5efa6e4ec0f87cf54fb14c85c3</citedby><cites>FETCH-LOGICAL-c381t-a2ba7a7ec7170103f346423ace93f8bbb97d6db5efa6e4ec0f87cf54fb14c85c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.lfs.2021.119387$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27926,27927,45997</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33774027$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Abdel-Fattah, Maha M.</creatorcontrib><creatorcontrib>Elgendy, Abdel Nasser.A.M.</creatorcontrib><creatorcontrib>Mohamed, Wafaa R.</creatorcontrib><title>Xanthenone, ACE2 activator, counteracted gentamicin-induced nephrotoxicity in rats: Impact on oxidative stress and ACE2/Ang-(1–7) signaling</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Nephrotoxicity is a rapid deterioration of kidney function due to exposure to nephrotoxic drugs as gentamicin. Gentamicin increases the generation of reactive oxygen species (ROS) leading to inflammatory responses and nuclear factor-κB (NF-κB) activation. The renal renin-angiotensin system (RAS) is considered a crucial regulator for physiological homeostasis and disease progression through the classic ACE/Ang-II/AT1 axis and its antagonist, ACE2/Ang-(1–7)/Mas axis which exerts an important role in the kidney. The present study evaluates the protective effects of the angiotensin-converting enzyme 2 (ACE2) activator; xanthenone; against experimental nephrotoxicity induced by gentamicin. Rats were divided into 4 groups, normal control, xanthenone (2 mg/kg, s.c), gentamicin (100 mg/kg, i.p. for one week) and xanthenone + gentamicin groups. Blood urea nitrogen (BUN) and serum creatinine levels were measured. The kidney tissues were used for estimating glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), NF-κB, Angiotensin II (AngII), and Ang-(1–7). In addition, histopathological examination and Western blot analysis of ACE2 expression were done. Xanthenone significantly restored serum levels of BUN and creatinine. Xanthenone exerted significant antioxidant effect as revealed by increased GSH content and SOD activity together with reduced MDA content. It exerted anti-inflammatory effect by significant reduction in TNF-α, NF-κB and IL-6 expression compared to gentamicin group. Xanthenone increased Ang-(1–7) and ACE2 expression while significantly decreased Ang-II expression. Histopathologically, xanthenone markedly counteracted gentamicin-induced renal aberrations. Activation of ACE2/Ang-(1–7) by xanthenone produced significant antioxidant and anti-inflammatory effects that counteracted gentamicin-induced nephrotoxicity.
[Display omitted]</description><subject>ACE2</subject><subject>ACE2 activator</subject><subject>Acute Kidney Injury - chemically induced</subject><subject>Acute Kidney Injury - prevention & control</subject><subject>Ang-(1–7)</subject><subject>Angiotensin</subject><subject>Angiotensin I - metabolism</subject><subject>Angiotensin II</subject><subject>Angiotensin-converting enzyme 2</subject><subject>Angiotensin-Converting Enzyme 2 - drug effects</subject><subject>Angiotensin-Converting Enzyme 2 - metabolism</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Blotting, Western</subject><subject>Creatinine</subject><subject>Gentamicin</subject><subject>Gentamicins - toxicity</subject><subject>Glutathione</subject><subject>Homeostasis</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Interleukins - metabolism</subject><subject>Kidneys</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Nephrotoxicity</subject><subject>NF-κB protein</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Peptide Fragments - metabolism</subject><subject>Peptidyl-dipeptidase A</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reactive oxygen species</subject><subject>Renin</subject><subject>Serum levels</subject><subject>Signal Transduction - drug effects</subject><subject>Superoxide dismutase</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Urea</subject><subject>Xanthenone</subject><subject>Xanthones - pharmacology</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UctKJDEUDaJo-_gANxJwM4LV5lFVqdJV0zijILhRcBdSqZs2TXfSJikZd_6AK__QL5k4rbOcVeDknHPvPQehQ0rGlND6bD5emDhmhNExpS1vxAYa0Ua0Bak53UQjQlhZcEaqHbQb45wQUlWCb6MdzoUoCRMj9PagXHoE5x2c4sn0kmGlk31WyYdTrP3gEoSMQI9n4JJaWm1dYV0_6Aw5WD0Gn_zvjKYXbB0OKsVzfL1cZQ32DuevXmU_wDEFiBEr1_8dczZxs-IH_Xh9Fyc42plTC-tm-2jLqEWEg693D93_vLybXhU3t7-up5ObQvOGpkKxTgklQAsqCCXc8LIuGVcaWm6aruta0dd9V4FRNZSgiWmENlVpOlrqptJ8Dx2vfVfBPw0Qk5z7IeQdomQVozlMwdrMomuWDj7GAEaugl2q8CIpkZ8FyLnMBcjPAuS6gKw5-nIeuiX0_xTfiWfCxZoA-b5nC0FGbcHlOG0AnWTv7X_s_wC7SZg9</recordid><startdate>20210615</startdate><enddate>20210615</enddate><creator>Abdel-Fattah, Maha M.</creator><creator>Elgendy, Abdel Nasser.A.M.</creator><creator>Mohamed, Wafaa R.</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></search><sort><creationdate>20210615</creationdate><title>Xanthenone, ACE2 activator, counteracted gentamicin-induced nephrotoxicity in rats: Impact on oxidative stress and ACE2/Ang-(1–7) signaling</title><author>Abdel-Fattah, Maha M. ; Elgendy, Abdel Nasser.A.M. ; Mohamed, Wafaa R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-a2ba7a7ec7170103f346423ace93f8bbb97d6db5efa6e4ec0f87cf54fb14c85c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>ACE2</topic><topic>ACE2 activator</topic><topic>Acute Kidney Injury - chemically induced</topic><topic>Acute Kidney Injury - prevention & control</topic><topic>Ang-(1–7)</topic><topic>Angiotensin</topic><topic>Angiotensin I - metabolism</topic><topic>Angiotensin II</topic><topic>Angiotensin-converting enzyme 2</topic><topic>Angiotensin-Converting Enzyme 2 - drug effects</topic><topic>Angiotensin-Converting Enzyme 2 - metabolism</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Blotting, Western</topic><topic>Creatinine</topic><topic>Gentamicin</topic><topic>Gentamicins - toxicity</topic><topic>Glutathione</topic><topic>Homeostasis</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Interleukins - metabolism</topic><topic>Kidneys</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Nephrotoxicity</topic><topic>NF-κB protein</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Peptide Fragments - metabolism</topic><topic>Peptidyl-dipeptidase A</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reactive oxygen species</topic><topic>Renin</topic><topic>Serum levels</topic><topic>Signal Transduction - drug effects</topic><topic>Superoxide dismutase</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Urea</topic><topic>Xanthenone</topic><topic>Xanthones - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Abdel-Fattah, Maha M.</creatorcontrib><creatorcontrib>Elgendy, Abdel Nasser.A.M.</creatorcontrib><creatorcontrib>Mohamed, Wafaa R.</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><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Abdel-Fattah, Maha M.</au><au>Elgendy, Abdel Nasser.A.M.</au><au>Mohamed, Wafaa R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Xanthenone, ACE2 activator, counteracted gentamicin-induced nephrotoxicity in rats: Impact on oxidative stress and ACE2/Ang-(1–7) signaling</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2021-06-15</date><risdate>2021</risdate><volume>275</volume><spage>119387</spage><pages>119387-</pages><artnum>119387</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Nephrotoxicity is a rapid deterioration of kidney function due to exposure to nephrotoxic drugs as gentamicin. Gentamicin increases the generation of reactive oxygen species (ROS) leading to inflammatory responses and nuclear factor-κB (NF-κB) activation. The renal renin-angiotensin system (RAS) is considered a crucial regulator for physiological homeostasis and disease progression through the classic ACE/Ang-II/AT1 axis and its antagonist, ACE2/Ang-(1–7)/Mas axis which exerts an important role in the kidney. The present study evaluates the protective effects of the angiotensin-converting enzyme 2 (ACE2) activator; xanthenone; against experimental nephrotoxicity induced by gentamicin. Rats were divided into 4 groups, normal control, xanthenone (2 mg/kg, s.c), gentamicin (100 mg/kg, i.p. for one week) and xanthenone + gentamicin groups. Blood urea nitrogen (BUN) and serum creatinine levels were measured. The kidney tissues were used for estimating glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), NF-κB, Angiotensin II (AngII), and Ang-(1–7). In addition, histopathological examination and Western blot analysis of ACE2 expression were done. Xanthenone significantly restored serum levels of BUN and creatinine. Xanthenone exerted significant antioxidant effect as revealed by increased GSH content and SOD activity together with reduced MDA content. It exerted anti-inflammatory effect by significant reduction in TNF-α, NF-κB and IL-6 expression compared to gentamicin group. Xanthenone increased Ang-(1–7) and ACE2 expression while significantly decreased Ang-II expression. Histopathologically, xanthenone markedly counteracted gentamicin-induced renal aberrations. Activation of ACE2/Ang-(1–7) by xanthenone produced significant antioxidant and anti-inflammatory effects that counteracted gentamicin-induced nephrotoxicity.
[Display omitted]</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>33774027</pmid><doi>10.1016/j.lfs.2021.119387</doi></addata></record> |
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| subjects | ACE2 ACE2 activator Acute Kidney Injury - chemically induced Acute Kidney Injury - prevention & control Ang-(1–7) Angiotensin Angiotensin I - metabolism Angiotensin II Angiotensin-converting enzyme 2 Angiotensin-Converting Enzyme 2 - drug effects Angiotensin-Converting Enzyme 2 - metabolism Animals Antioxidants Blotting, Western Creatinine Gentamicin Gentamicins - toxicity Glutathione Homeostasis Inflammation Interleukin 6 Interleukins - metabolism Kidneys Male Malondialdehyde Nephrotoxicity NF-κB protein Oxidative stress Oxidative Stress - drug effects Peptide Fragments - metabolism Peptidyl-dipeptidase A Rats Rats, Wistar Reactive oxygen species Renin Serum levels Signal Transduction - drug effects Superoxide dismutase Tumor necrosis factor-TNF Tumor necrosis factor-α Urea Xanthenone Xanthones - pharmacology |
| title | Xanthenone, ACE2 activator, counteracted gentamicin-induced nephrotoxicity in rats: Impact on oxidative stress and ACE2/Ang-(1–7) signaling |
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