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Renal protective effects of thymoquinone against sodium nitrite-induced chronic toxicity in rats: Impact on inflammation and apoptosis
Sodium nitrite is a widely used color fixative and preservative. However, it has been reported to exert deleterious toxic effects on various body organs. Moreover, thymoquinone (TQ), the active constituent of Nigella sativa oil is known to possess beneficial antioxidant and anti-inflammatory effects...
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Published in: | Life sciences (1973) 2017-07, Vol.180, p.1-8 |
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description | Sodium nitrite is a widely used color fixative and preservative. However, it has been reported to exert deleterious toxic effects on various body organs. Moreover, thymoquinone (TQ), the active constituent of Nigella sativa oil is known to possess beneficial antioxidant and anti-inflammatory effects. The present study was conducted to evaluate the potential protective effects of TQ against sodium nitrite-induced renal toxicity.
Male Sprague-Dawley rats were treated with sodium nitrite (80mg/kg, po, daily) in presence or absence of TQ (25 and 50mg/kg, po, daily). Morphological changes in renal sections were assessed by staining with Hematoxylin/Eosin and Periodic acid–Schiff. Renal homogenate was used for measurement of oxidative stress markers (MDA and GSH), inflammatory markers (CRP, TNF-α, IL-6, IL-1β), anti-inflammatory cytokines (IL-10 and IL-4) and apoptotic markers (caspase-3/caspase-8/caspase-9).
Treatment with sodium nitrite significantly increased markers of renal dysfunction, oxidative stress, inflammation and apoptosis. These effects were markedly attenuated by TQ in dose dependent manner.
TQ has a potential protective effect against sodium nitrite-induced renal toxicity. This can be attributed to its ability to dampen oxidative stress, restore the normal balance between pro- and anti-inflammatory cytokines and protect renal tissue form extrinsic and intrinsic apoptosis.
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doi_str_mv | 10.1016/j.lfs.2017.05.005 |
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Male Sprague-Dawley rats were treated with sodium nitrite (80mg/kg, po, daily) in presence or absence of TQ (25 and 50mg/kg, po, daily). Morphological changes in renal sections were assessed by staining with Hematoxylin/Eosin and Periodic acid–Schiff. Renal homogenate was used for measurement of oxidative stress markers (MDA and GSH), inflammatory markers (CRP, TNF-α, IL-6, IL-1β), anti-inflammatory cytokines (IL-10 and IL-4) and apoptotic markers (caspase-3/caspase-8/caspase-9).
Treatment with sodium nitrite significantly increased markers of renal dysfunction, oxidative stress, inflammation and apoptosis. These effects were markedly attenuated by TQ in dose dependent manner.
TQ has a potential protective effect against sodium nitrite-induced renal toxicity. This can be attributed to its ability to dampen oxidative stress, restore the normal balance between pro- and anti-inflammatory cytokines and protect renal tissue form extrinsic and intrinsic apoptosis.
[Display omitted]</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2017.05.005</identifier><identifier>PMID: 28495515</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Animals ; Antioxidants ; Apoptosis ; Apoptosis - drug effects ; Benzoquinones - administration & dosage ; Benzoquinones - pharmacology ; Caspase ; Caspase-3 ; Caspase-8 ; Caspase-9 ; Chronic toxicity ; Cytokines ; Cytokines - metabolism ; Dose-Response Relationship, Drug ; Food Preservatives - toxicity ; Inflammation ; Inflammation - chemically induced ; Inflammation - pathology ; Inflammation - prevention & control ; Inflammation and apoptosis ; Inflammation Mediators - metabolism ; Interleukin 10 ; Interleukin 4 ; Interleukin 6 ; Kidney Diseases - chemically induced ; Kidney Diseases - pathology ; Kidney Diseases - prevention & control ; Male ; Markers ; Nephrotoxicity ; Nitrites ; Organs ; Oxidative stress ; Oxidative Stress - drug effects ; Rats ; Rats, Sprague-Dawley ; Renal function ; Sodium ; Sodium nitrite ; Sodium Nitrite - toxicity ; Studies ; Thymoquinone ; Toxicity ; Tumor necrosis factor</subject><ispartof>Life sciences (1973), 2017-07, Vol.180, p.1-8</ispartof><rights>2017 Elsevier Inc.</rights><rights>Copyright © 2017 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Jul 1, 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-4d0572b9e80d92d1c9ded7486c84247f66f93eef7db532503408e7ba80c10d703</citedby><cites>FETCH-LOGICAL-c447t-4d0572b9e80d92d1c9ded7486c84247f66f93eef7db532503408e7ba80c10d703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28495515$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Elsherbiny, Nehal M.</creatorcontrib><creatorcontrib>Maysarah, Nadia M.</creatorcontrib><creatorcontrib>El-Sherbiny, Mohamed</creatorcontrib><creatorcontrib>Al-Gayyar, Mohamed M.</creatorcontrib><title>Renal protective effects of thymoquinone against sodium nitrite-induced chronic toxicity in rats: Impact on inflammation and apoptosis</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Sodium nitrite is a widely used color fixative and preservative. However, it has been reported to exert deleterious toxic effects on various body organs. Moreover, thymoquinone (TQ), the active constituent of Nigella sativa oil is known to possess beneficial antioxidant and anti-inflammatory effects. The present study was conducted to evaluate the potential protective effects of TQ against sodium nitrite-induced renal toxicity.
Male Sprague-Dawley rats were treated with sodium nitrite (80mg/kg, po, daily) in presence or absence of TQ (25 and 50mg/kg, po, daily). Morphological changes in renal sections were assessed by staining with Hematoxylin/Eosin and Periodic acid–Schiff. Renal homogenate was used for measurement of oxidative stress markers (MDA and GSH), inflammatory markers (CRP, TNF-α, IL-6, IL-1β), anti-inflammatory cytokines (IL-10 and IL-4) and apoptotic markers (caspase-3/caspase-8/caspase-9).
Treatment with sodium nitrite significantly increased markers of renal dysfunction, oxidative stress, inflammation and apoptosis. These effects were markedly attenuated by TQ in dose dependent manner.
TQ has a potential protective effect against sodium nitrite-induced renal toxicity. This can be attributed to its ability to dampen oxidative stress, restore the normal balance between pro- and anti-inflammatory cytokines and protect renal tissue form extrinsic and intrinsic apoptosis.
[Display omitted]</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Benzoquinones - administration & dosage</subject><subject>Benzoquinones - pharmacology</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Caspase-8</subject><subject>Caspase-9</subject><subject>Chronic toxicity</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Food Preservatives - toxicity</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - pathology</subject><subject>Inflammation - prevention & control</subject><subject>Inflammation and apoptosis</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin 10</subject><subject>Interleukin 4</subject><subject>Interleukin 6</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - pathology</subject><subject>Kidney Diseases - prevention & control</subject><subject>Male</subject><subject>Markers</subject><subject>Nephrotoxicity</subject><subject>Nitrites</subject><subject>Organs</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renal function</subject><subject>Sodium</subject><subject>Sodium nitrite</subject><subject>Sodium Nitrite - toxicity</subject><subject>Studies</subject><subject>Thymoquinone</subject><subject>Toxicity</subject><subject>Tumor necrosis factor</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp9kM9qFTEUh4NY7G31AdxIwPWMJzPJZEZXUtQWCoVS1yE3ObG53EmmSab0voDPbcqtLl2dP3znB-cj5D2DlgEbPu3avcttB0y2IFoA8Yps2CinBoaevSYbgI43fQfilJzlvINKCNm_IafdyCchmNiQ37cY9J4uKRY0xT8iRedql2l0tNwf5viw-hADUv1L-5ALzdH6dabBl-QLNj7Y1aCl5j7F4A0t8ckbXw7UB5p0yZ_p1bxoU2gMdeX2ep518XXQwVK9xKXE7PNbcuL0PuO7l3pOfn7_dndx2Vzf_Li6-HrdGM5labgFIbvthCPYqbPMTBat5ONgRt5x6YbBTT2ik3Yr-k5Az2FEudUjGAZWQn9OPh5z68MPK-aidnFN1UBWbOKdZDD1Q6XYkTIp5pzQqSX5WaeDYqCezaudqubVs3kFQlWv9ebDS_K6ndH-u_irugJfjgDW_x49JpWNx1Dd-VSFKxv9f-L_AJdQlnk</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Elsherbiny, Nehal M.</creator><creator>Maysarah, Nadia M.</creator><creator>El-Sherbiny, Mohamed</creator><creator>Al-Gayyar, Mohamed M.</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>20170701</creationdate><title>Renal protective effects of thymoquinone against sodium nitrite-induced chronic toxicity in rats: Impact on inflammation and apoptosis</title><author>Elsherbiny, Nehal M. ; Maysarah, Nadia M. ; El-Sherbiny, Mohamed ; Al-Gayyar, Mohamed M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-4d0572b9e80d92d1c9ded7486c84247f66f93eef7db532503408e7ba80c10d703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Benzoquinones - administration & dosage</topic><topic>Benzoquinones - pharmacology</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Caspase-8</topic><topic>Caspase-9</topic><topic>Chronic toxicity</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Food Preservatives - toxicity</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - pathology</topic><topic>Inflammation - prevention & control</topic><topic>Inflammation and apoptosis</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin 10</topic><topic>Interleukin 4</topic><topic>Interleukin 6</topic><topic>Kidney Diseases - chemically induced</topic><topic>Kidney Diseases - pathology</topic><topic>Kidney Diseases - prevention & control</topic><topic>Male</topic><topic>Markers</topic><topic>Nephrotoxicity</topic><topic>Nitrites</topic><topic>Organs</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renal function</topic><topic>Sodium</topic><topic>Sodium nitrite</topic><topic>Sodium Nitrite - toxicity</topic><topic>Studies</topic><topic>Thymoquinone</topic><topic>Toxicity</topic><topic>Tumor necrosis factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Elsherbiny, Nehal M.</creatorcontrib><creatorcontrib>Maysarah, Nadia M.</creatorcontrib><creatorcontrib>El-Sherbiny, Mohamed</creatorcontrib><creatorcontrib>Al-Gayyar, Mohamed M.</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>Elsherbiny, Nehal M.</au><au>Maysarah, Nadia M.</au><au>El-Sherbiny, Mohamed</au><au>Al-Gayyar, Mohamed M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Renal protective effects of thymoquinone against sodium nitrite-induced chronic toxicity in rats: Impact on inflammation and apoptosis</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>180</volume><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Sodium nitrite is a widely used color fixative and preservative. However, it has been reported to exert deleterious toxic effects on various body organs. Moreover, thymoquinone (TQ), the active constituent of Nigella sativa oil is known to possess beneficial antioxidant and anti-inflammatory effects. The present study was conducted to evaluate the potential protective effects of TQ against sodium nitrite-induced renal toxicity.
Male Sprague-Dawley rats were treated with sodium nitrite (80mg/kg, po, daily) in presence or absence of TQ (25 and 50mg/kg, po, daily). Morphological changes in renal sections were assessed by staining with Hematoxylin/Eosin and Periodic acid–Schiff. Renal homogenate was used for measurement of oxidative stress markers (MDA and GSH), inflammatory markers (CRP, TNF-α, IL-6, IL-1β), anti-inflammatory cytokines (IL-10 and IL-4) and apoptotic markers (caspase-3/caspase-8/caspase-9).
Treatment with sodium nitrite significantly increased markers of renal dysfunction, oxidative stress, inflammation and apoptosis. These effects were markedly attenuated by TQ in dose dependent manner.
TQ has a potential protective effect against sodium nitrite-induced renal toxicity. This can be attributed to its ability to dampen oxidative stress, restore the normal balance between pro- and anti-inflammatory cytokines and protect renal tissue form extrinsic and intrinsic apoptosis.
[Display omitted]</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>28495515</pmid><doi>10.1016/j.lfs.2017.05.005</doi><tpages>8</tpages></addata></record> |
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subjects | Animals Antioxidants Apoptosis Apoptosis - drug effects Benzoquinones - administration & dosage Benzoquinones - pharmacology Caspase Caspase-3 Caspase-8 Caspase-9 Chronic toxicity Cytokines Cytokines - metabolism Dose-Response Relationship, Drug Food Preservatives - toxicity Inflammation Inflammation - chemically induced Inflammation - pathology Inflammation - prevention & control Inflammation and apoptosis Inflammation Mediators - metabolism Interleukin 10 Interleukin 4 Interleukin 6 Kidney Diseases - chemically induced Kidney Diseases - pathology Kidney Diseases - prevention & control Male Markers Nephrotoxicity Nitrites Organs Oxidative stress Oxidative Stress - drug effects Rats Rats, Sprague-Dawley Renal function Sodium Sodium nitrite Sodium Nitrite - toxicity Studies Thymoquinone Toxicity Tumor necrosis factor |
title | Renal protective effects of thymoquinone against sodium nitrite-induced chronic toxicity in rats: Impact on inflammation and apoptosis |
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