10-Dehydrogingerdione ameliorates renal endoplasmic reticulum/oxidative stress and apoptosis in alcoholic nephropathy induced in experimental rats
Chronic alcoholism induces kidney injury (KI), leading to increased mortality in alcoholic hepatitis patients. Endoplasmic reticulum stress (ER) represents the main initiator of kidney diseases and alcoholic nephropathy. We used alcoholic nephropathy rat model followed by 10-dehydrogingerdione (10-D...
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| Veröffentlicht in: | Life sciences (1973) 2021-08, Vol.279, p.119673, Article 119673 |
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| creator | Elnagar, Gehad M. Elseweidy, Mohamed M. Elkomy, Nesreen M.I.M. Al-Gabri, Naif A. Shawky, Mohamed |
| description | Chronic alcoholism induces kidney injury (KI), leading to increased mortality in alcoholic hepatitis patients. Endoplasmic reticulum stress (ER) represents the main initiator of kidney diseases and alcoholic nephropathy.
We used alcoholic nephropathy rat model followed by 10-dehydrogingerdione (10-DHGD) intake as potential modulator. This is to focus on ER/oxidative stress/inflammatory and apoptotic pathways involvement.
Alcoholic nephropathy was induced by alcohol administration (3.7 g/kg/body weight) orally and daily for 45 days. 10-DHGD (10 mg/kg/day) was administered either alone or along with alcohol.
Our results demonstrated significant increase in kidney function parameters like f creatinine, urea, uric acid, and blood urea nitrogen (BUN) levels. Renal ER/oxidative stress markers such as cytochrome P450 family two subfamily E member 1 (CYP2E1), C/EBP homologous protein (CHOP), and endoplasmic glucose-regulated protein 78 (GRP-78) demonstrated also significant increase. Inflammatory mediators like nuclear factor-kappa B (NF-kB), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β along with apoptotic marker caspase-3 behaved similarly. Antioxidant molecules like reduced glutathione (GSH), superoxide dismutase (SOD), and catalase demonstrated marked decrease.
10-DHGD administration resulted in significant modulation represented by an enhancement in the kidney functions and the histopathological patterns in a conclusion of its potential to ameliorate the pathological changes (kidney injury) induced by alcohol intake.
[Display omitted]
•Chronic alcoholism mediated nephrotoxicity in rats.•New insights of chronic alcoholism induced kidney injury.•10-DHGD protects against alcohol induced neuropathy via inhibition of renal endoplasmic reticulum /oxidative stress /inflammatory and apoptotic pathways. |
| doi_str_mv | 10.1016/j.lfs.2021.119673 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2551712400</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0024320521006597</els_id><sourcerecordid>2551712400</sourcerecordid><originalsourceid>FETCH-LOGICAL-c381t-8b71c3678b7cfc7732e08aefadca6f30a18795516fdfd2d8feaa71135e3ac6a33</originalsourceid><addsrcrecordid>eNp9UcFO3DAQtaqistB-QC9VpJ6zeOJNnBWnCmhBQuJCz9Zgj1mvEju1HcT-Bl-MVws9chpp5r03M-8x9h34Ejh0Z9vlYNOy4Q0sAdadFJ_YAnq5rnkn4DNbcN6satHw9pidpLTlnLetFF_YsVjxHtZrWLAX4PUlbXYmhkfnHykaFzxVONLgQsRMqYrkcajImzANmEanSyc7PQ_zeBaencHsnqhKOVJKFXpT4RSmHJJLlfMVDjpswlBYnqZNDBPmza4MzKzJ7AH0PFF0I_lctpSN6Ss7sjgk-vZWT9nf31f3F9f17d2fm4tft7UWPeS6f5CgRSdL1VZLKRriPZJFo7GzguPeibaFzhprGtNbQpQAoiWBukMhTtnPg-4Uw7-ZUlbbMMfya1JN4UloVpwXFBxQOoaUIlk1lWsx7hRwtU9BbVVJQe1TUIcUCufHm_L8MJL5z3i3vQDODwAq_z05iippR7444iLprExwH8i_AosznHw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2551712400</pqid></control><display><type>article</type><title>10-Dehydrogingerdione ameliorates renal endoplasmic reticulum/oxidative stress and apoptosis in alcoholic nephropathy induced in experimental rats</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Elnagar, Gehad M. ; Elseweidy, Mohamed M. ; Elkomy, Nesreen M.I.M. ; Al-Gabri, Naif A. ; Shawky, Mohamed</creator><creatorcontrib>Elnagar, Gehad M. ; Elseweidy, Mohamed M. ; Elkomy, Nesreen M.I.M. ; Al-Gabri, Naif A. ; Shawky, Mohamed</creatorcontrib><description>Chronic alcoholism induces kidney injury (KI), leading to increased mortality in alcoholic hepatitis patients. Endoplasmic reticulum stress (ER) represents the main initiator of kidney diseases and alcoholic nephropathy.
We used alcoholic nephropathy rat model followed by 10-dehydrogingerdione (10-DHGD) intake as potential modulator. This is to focus on ER/oxidative stress/inflammatory and apoptotic pathways involvement.
Alcoholic nephropathy was induced by alcohol administration (3.7 g/kg/body weight) orally and daily for 45 days. 10-DHGD (10 mg/kg/day) was administered either alone or along with alcohol.
Our results demonstrated significant increase in kidney function parameters like f creatinine, urea, uric acid, and blood urea nitrogen (BUN) levels. Renal ER/oxidative stress markers such as cytochrome P450 family two subfamily E member 1 (CYP2E1), C/EBP homologous protein (CHOP), and endoplasmic glucose-regulated protein 78 (GRP-78) demonstrated also significant increase. Inflammatory mediators like nuclear factor-kappa B (NF-kB), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β along with apoptotic marker caspase-3 behaved similarly. Antioxidant molecules like reduced glutathione (GSH), superoxide dismutase (SOD), and catalase demonstrated marked decrease.
10-DHGD administration resulted in significant modulation represented by an enhancement in the kidney functions and the histopathological patterns in a conclusion of its potential to ameliorate the pathological changes (kidney injury) induced by alcohol intake.
[Display omitted]
•Chronic alcoholism mediated nephrotoxicity in rats.•New insights of chronic alcoholism induced kidney injury.•10-DHGD protects against alcohol induced neuropathy via inhibition of renal endoplasmic reticulum /oxidative stress /inflammatory and apoptotic pathways.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2021.119673</identifier><identifier>PMID: 34081991</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>10-Dehydrogingerdione ; Alcohol ; Alcoholic beverages ; Alcoholism ; Alcoholism - drug therapy ; Alcoholism - etiology ; Alcoholism - pathology ; Animals ; Antioxidants ; Apoptosis ; Body weight ; Caspase-3 ; Catalase ; CCAAT/enhancer-binding protein ; Central Nervous System Depressants - toxicity ; Creatinine ; Cytochrome ; Cytochrome P450 ; Cytochromes P450 ; Drug abuse ; Endoplasmic reticulum ; Endoplasmic reticulum stress ; Endoplasmic Reticulum Stress - drug effects ; Ethanol - toxicity ; Glutathione ; Growth factors ; Guaiacol - analogs & derivatives ; Guaiacol - pharmacology ; Hepatitis ; Homology ; Inflammation ; Inflammatory and apoptosis markers ; Kidney diseases ; Kidney Diseases - chemically induced ; Kidney Diseases - drug therapy ; Kidney Diseases - pathology ; Kidneys ; Male ; Markers ; Nephropathy ; NF-κB protein ; Oxidative stress ; Oxidative Stress - drug effects ; Proteins ; Rats ; Superoxide dismutase ; Transforming growth factor-b ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Urea ; Uric acid</subject><ispartof>Life sciences (1973), 2021-08, Vol.279, p.119673, Article 119673</ispartof><rights>2021 Elsevier Inc.</rights><rights>Copyright © 2021 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Aug 15, 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-8b71c3678b7cfc7732e08aefadca6f30a18795516fdfd2d8feaa71135e3ac6a33</citedby><cites>FETCH-LOGICAL-c381t-8b71c3678b7cfc7732e08aefadca6f30a18795516fdfd2d8feaa71135e3ac6a33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0024320521006597$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34081991$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Elnagar, Gehad M.</creatorcontrib><creatorcontrib>Elseweidy, Mohamed M.</creatorcontrib><creatorcontrib>Elkomy, Nesreen M.I.M.</creatorcontrib><creatorcontrib>Al-Gabri, Naif A.</creatorcontrib><creatorcontrib>Shawky, Mohamed</creatorcontrib><title>10-Dehydrogingerdione ameliorates renal endoplasmic reticulum/oxidative stress and apoptosis in alcoholic nephropathy induced in experimental rats</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Chronic alcoholism induces kidney injury (KI), leading to increased mortality in alcoholic hepatitis patients. Endoplasmic reticulum stress (ER) represents the main initiator of kidney diseases and alcoholic nephropathy.
We used alcoholic nephropathy rat model followed by 10-dehydrogingerdione (10-DHGD) intake as potential modulator. This is to focus on ER/oxidative stress/inflammatory and apoptotic pathways involvement.
Alcoholic nephropathy was induced by alcohol administration (3.7 g/kg/body weight) orally and daily for 45 days. 10-DHGD (10 mg/kg/day) was administered either alone or along with alcohol.
Our results demonstrated significant increase in kidney function parameters like f creatinine, urea, uric acid, and blood urea nitrogen (BUN) levels. Renal ER/oxidative stress markers such as cytochrome P450 family two subfamily E member 1 (CYP2E1), C/EBP homologous protein (CHOP), and endoplasmic glucose-regulated protein 78 (GRP-78) demonstrated also significant increase. Inflammatory mediators like nuclear factor-kappa B (NF-kB), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β along with apoptotic marker caspase-3 behaved similarly. Antioxidant molecules like reduced glutathione (GSH), superoxide dismutase (SOD), and catalase demonstrated marked decrease.
10-DHGD administration resulted in significant modulation represented by an enhancement in the kidney functions and the histopathological patterns in a conclusion of its potential to ameliorate the pathological changes (kidney injury) induced by alcohol intake.
[Display omitted]
•Chronic alcoholism mediated nephrotoxicity in rats.•New insights of chronic alcoholism induced kidney injury.•10-DHGD protects against alcohol induced neuropathy via inhibition of renal endoplasmic reticulum /oxidative stress /inflammatory and apoptotic pathways.</description><subject>10-Dehydrogingerdione</subject><subject>Alcohol</subject><subject>Alcoholic beverages</subject><subject>Alcoholism</subject><subject>Alcoholism - drug therapy</subject><subject>Alcoholism - etiology</subject><subject>Alcoholism - pathology</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Body weight</subject><subject>Caspase-3</subject><subject>Catalase</subject><subject>CCAAT/enhancer-binding protein</subject><subject>Central Nervous System Depressants - toxicity</subject><subject>Creatinine</subject><subject>Cytochrome</subject><subject>Cytochrome P450</subject><subject>Cytochromes P450</subject><subject>Drug abuse</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic reticulum stress</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>Ethanol - toxicity</subject><subject>Glutathione</subject><subject>Growth factors</subject><subject>Guaiacol - analogs & derivatives</subject><subject>Guaiacol - pharmacology</subject><subject>Hepatitis</subject><subject>Homology</subject><subject>Inflammation</subject><subject>Inflammatory and apoptosis markers</subject><subject>Kidney diseases</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - drug therapy</subject><subject>Kidney Diseases - pathology</subject><subject>Kidneys</subject><subject>Male</subject><subject>Markers</subject><subject>Nephropathy</subject><subject>NF-κB protein</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Proteins</subject><subject>Rats</subject><subject>Superoxide dismutase</subject><subject>Transforming growth factor-b</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Urea</subject><subject>Uric acid</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>eNp9UcFO3DAQtaqistB-QC9VpJ6zeOJNnBWnCmhBQuJCz9Zgj1mvEju1HcT-Bl-MVws9chpp5r03M-8x9h34Ejh0Z9vlYNOy4Q0sAdadFJ_YAnq5rnkn4DNbcN6satHw9pidpLTlnLetFF_YsVjxHtZrWLAX4PUlbXYmhkfnHykaFzxVONLgQsRMqYrkcajImzANmEanSyc7PQ_zeBaencHsnqhKOVJKFXpT4RSmHJJLlfMVDjpswlBYnqZNDBPmza4MzKzJ7AH0PFF0I_lctpSN6Ss7sjgk-vZWT9nf31f3F9f17d2fm4tft7UWPeS6f5CgRSdL1VZLKRriPZJFo7GzguPeibaFzhprGtNbQpQAoiWBukMhTtnPg-4Uw7-ZUlbbMMfya1JN4UloVpwXFBxQOoaUIlk1lWsx7hRwtU9BbVVJQe1TUIcUCufHm_L8MJL5z3i3vQDODwAq_z05iippR7444iLprExwH8i_AosznHw</recordid><startdate>20210815</startdate><enddate>20210815</enddate><creator>Elnagar, Gehad M.</creator><creator>Elseweidy, Mohamed M.</creator><creator>Elkomy, Nesreen M.I.M.</creator><creator>Al-Gabri, Naif A.</creator><creator>Shawky, Mohamed</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>20210815</creationdate><title>10-Dehydrogingerdione ameliorates renal endoplasmic reticulum/oxidative stress and apoptosis in alcoholic nephropathy induced in experimental rats</title><author>Elnagar, Gehad M. ; Elseweidy, Mohamed M. ; Elkomy, Nesreen M.I.M. ; Al-Gabri, Naif A. ; Shawky, Mohamed</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-8b71c3678b7cfc7732e08aefadca6f30a18795516fdfd2d8feaa71135e3ac6a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>10-Dehydrogingerdione</topic><topic>Alcohol</topic><topic>Alcoholic beverages</topic><topic>Alcoholism</topic><topic>Alcoholism - drug therapy</topic><topic>Alcoholism - etiology</topic><topic>Alcoholism - pathology</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Body weight</topic><topic>Caspase-3</topic><topic>Catalase</topic><topic>CCAAT/enhancer-binding protein</topic><topic>Central Nervous System Depressants - toxicity</topic><topic>Creatinine</topic><topic>Cytochrome</topic><topic>Cytochrome P450</topic><topic>Cytochromes P450</topic><topic>Drug abuse</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic reticulum stress</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>Ethanol - toxicity</topic><topic>Glutathione</topic><topic>Growth factors</topic><topic>Guaiacol - analogs & derivatives</topic><topic>Guaiacol - pharmacology</topic><topic>Hepatitis</topic><topic>Homology</topic><topic>Inflammation</topic><topic>Inflammatory and apoptosis markers</topic><topic>Kidney diseases</topic><topic>Kidney Diseases - chemically induced</topic><topic>Kidney Diseases - drug therapy</topic><topic>Kidney Diseases - pathology</topic><topic>Kidneys</topic><topic>Male</topic><topic>Markers</topic><topic>Nephropathy</topic><topic>NF-κB protein</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Proteins</topic><topic>Rats</topic><topic>Superoxide dismutase</topic><topic>Transforming growth factor-b</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Urea</topic><topic>Uric acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Elnagar, Gehad M.</creatorcontrib><creatorcontrib>Elseweidy, Mohamed M.</creatorcontrib><creatorcontrib>Elkomy, Nesreen M.I.M.</creatorcontrib><creatorcontrib>Al-Gabri, Naif A.</creatorcontrib><creatorcontrib>Shawky, Mohamed</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>Elnagar, Gehad M.</au><au>Elseweidy, Mohamed M.</au><au>Elkomy, Nesreen M.I.M.</au><au>Al-Gabri, Naif A.</au><au>Shawky, Mohamed</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>10-Dehydrogingerdione ameliorates renal endoplasmic reticulum/oxidative stress and apoptosis in alcoholic nephropathy induced in experimental rats</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2021-08-15</date><risdate>2021</risdate><volume>279</volume><spage>119673</spage><pages>119673-</pages><artnum>119673</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Chronic alcoholism induces kidney injury (KI), leading to increased mortality in alcoholic hepatitis patients. Endoplasmic reticulum stress (ER) represents the main initiator of kidney diseases and alcoholic nephropathy.
We used alcoholic nephropathy rat model followed by 10-dehydrogingerdione (10-DHGD) intake as potential modulator. This is to focus on ER/oxidative stress/inflammatory and apoptotic pathways involvement.
Alcoholic nephropathy was induced by alcohol administration (3.7 g/kg/body weight) orally and daily for 45 days. 10-DHGD (10 mg/kg/day) was administered either alone or along with alcohol.
Our results demonstrated significant increase in kidney function parameters like f creatinine, urea, uric acid, and blood urea nitrogen (BUN) levels. Renal ER/oxidative stress markers such as cytochrome P450 family two subfamily E member 1 (CYP2E1), C/EBP homologous protein (CHOP), and endoplasmic glucose-regulated protein 78 (GRP-78) demonstrated also significant increase. Inflammatory mediators like nuclear factor-kappa B (NF-kB), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β along with apoptotic marker caspase-3 behaved similarly. Antioxidant molecules like reduced glutathione (GSH), superoxide dismutase (SOD), and catalase demonstrated marked decrease.
10-DHGD administration resulted in significant modulation represented by an enhancement in the kidney functions and the histopathological patterns in a conclusion of its potential to ameliorate the pathological changes (kidney injury) induced by alcohol intake.
[Display omitted]
•Chronic alcoholism mediated nephrotoxicity in rats.•New insights of chronic alcoholism induced kidney injury.•10-DHGD protects against alcohol induced neuropathy via inhibition of renal endoplasmic reticulum /oxidative stress /inflammatory and apoptotic pathways.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>34081991</pmid><doi>10.1016/j.lfs.2021.119673</doi></addata></record> |
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| subjects | 10-Dehydrogingerdione Alcohol Alcoholic beverages Alcoholism Alcoholism - drug therapy Alcoholism - etiology Alcoholism - pathology Animals Antioxidants Apoptosis Body weight Caspase-3 Catalase CCAAT/enhancer-binding protein Central Nervous System Depressants - toxicity Creatinine Cytochrome Cytochrome P450 Cytochromes P450 Drug abuse Endoplasmic reticulum Endoplasmic reticulum stress Endoplasmic Reticulum Stress - drug effects Ethanol - toxicity Glutathione Growth factors Guaiacol - analogs & derivatives Guaiacol - pharmacology Hepatitis Homology Inflammation Inflammatory and apoptosis markers Kidney diseases Kidney Diseases - chemically induced Kidney Diseases - drug therapy Kidney Diseases - pathology Kidneys Male Markers Nephropathy NF-κB protein Oxidative stress Oxidative Stress - drug effects Proteins Rats Superoxide dismutase Transforming growth factor-b Tumor necrosis factor-TNF Tumor necrosis factor-α Urea Uric acid |
| title | 10-Dehydrogingerdione ameliorates renal endoplasmic reticulum/oxidative stress and apoptosis in alcoholic nephropathy induced in experimental rats |
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