Cross-Regulation between Autophagy and Apoptosis Induced by Vitamin E and Lactobacillus Plantarum through Beclin-1 Network
Autophagy and apoptosis are two important regulatory mechanisms for how the body can respond to diseases. This study was designed to investigate the protective actions of vitamin E (Vit-E) and lactobacillus plantarum (Lac-B) against mercuric chloride (HgCl )-induced kidney injury. Thirty albino rats...
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| Veröffentlicht in: | International journal of molecular sciences 2022-12, Vol.23 (23), p.15305 |
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| creator | Alhusaini, Ahlam M Alhumaidan, Sara A Alharbi, Ghaida M Alzahrani, Eman A Sarawi, Wedad S Alomar, Hatun A Alanazi, Abeer M Mattar, Dareen S Hasan, Iman H |
| description | Autophagy and apoptosis are two important regulatory mechanisms for how the body can respond to diseases. This study was designed to investigate the protective actions of vitamin E (Vit-E) and lactobacillus plantarum (Lac-B) against mercuric chloride (HgCl
)-induced kidney injury. Thirty albino rats were divided into five groups: group 1 served as the normal group; rats in group 2 received high doses of HgCl
; rats in groups 3, 4 and 5 were given Vit-E, Lac-B and the combination of Vit-E and Lac-B, respectively along with HgCl
for two weeks. HgCl
provoked renal injury, manifested by elevation in serum urea, urea nitrogen and creatinine. Kidney levels of oxidative stress and inflammation were markedly increased post HgCl
administration. Moreover, HgCl
significantly elevated the gene expression levels of VCAM-1 and cystatin
, while podocin was downregulated. Additionally, it markedly decreased the protein expression of Beclin-1 and Bcl-2. Histopathological examination revealed massive degeneration with congested blood vessels following HgCl
administration. Treatment with Vit-E or/and Lac-B restored the normal levels of the previously mentioned parameters, as well as improved the morphology of kidney tissues. Both Vit-E and Lac-B provided a protective effect against HgCl
-induced kidney damage by regulating autophagy and apoptosis. |
| doi_str_mv | 10.3390/ijms232315305 |
| format | Article |
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)-induced kidney injury. Thirty albino rats were divided into five groups: group 1 served as the normal group; rats in group 2 received high doses of HgCl
; rats in groups 3, 4 and 5 were given Vit-E, Lac-B and the combination of Vit-E and Lac-B, respectively along with HgCl
for two weeks. HgCl
provoked renal injury, manifested by elevation in serum urea, urea nitrogen and creatinine. Kidney levels of oxidative stress and inflammation were markedly increased post HgCl
administration. Moreover, HgCl
significantly elevated the gene expression levels of VCAM-1 and cystatin
, while podocin was downregulated. Additionally, it markedly decreased the protein expression of Beclin-1 and Bcl-2. Histopathological examination revealed massive degeneration with congested blood vessels following HgCl
administration. Treatment with Vit-E or/and Lac-B restored the normal levels of the previously mentioned parameters, as well as improved the morphology of kidney tissues. Both Vit-E and Lac-B provided a protective effect against HgCl
-induced kidney damage by regulating autophagy and apoptosis.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms232315305</identifier><identifier>PMID: 36499631</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Antioxidants ; Antioxidants - pharmacology ; Apoptosis ; Autophagy ; Bcl-2 protein ; Beclin-1 - metabolism ; Blood vessels ; Creatinine ; Cystatin C ; Degeneration ; Gene expression ; Homeostasis ; Intoxication ; Kidney - metabolism ; Kidneys ; Lactobacilli ; Lactobacillus plantarum - metabolism ; Mercuric chloride ; Mercuric Chloride - toxicity ; Mercury compounds ; Oxidative Stress ; Protein expression ; Proteins ; Rats ; Tocopherol ; Urea - pharmacology ; Ureas ; Vascular cell adhesion molecule 1 ; Vitamin E ; Vitamin E - metabolism ; Vitamin E - pharmacology</subject><ispartof>International journal of molecular sciences, 2022-12, Vol.23 (23), p.15305</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c371t-ca56adc3f4e397e9bd4d2406fe1d7d9dc75bdb06b0d5382390305f312508cd863</cites><orcidid>0000-0001-7495-0592 ; 0000-0003-2905-8882 ; 0000-0001-6376-9464 ; 0000-0001-7311-1412</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9736033/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9736033/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27911,27912,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36499631$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alhusaini, Ahlam M</creatorcontrib><creatorcontrib>Alhumaidan, Sara A</creatorcontrib><creatorcontrib>Alharbi, Ghaida M</creatorcontrib><creatorcontrib>Alzahrani, Eman A</creatorcontrib><creatorcontrib>Sarawi, Wedad S</creatorcontrib><creatorcontrib>Alomar, Hatun A</creatorcontrib><creatorcontrib>Alanazi, Abeer M</creatorcontrib><creatorcontrib>Mattar, Dareen S</creatorcontrib><creatorcontrib>Hasan, Iman H</creatorcontrib><title>Cross-Regulation between Autophagy and Apoptosis Induced by Vitamin E and Lactobacillus Plantarum through Beclin-1 Network</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Autophagy and apoptosis are two important regulatory mechanisms for how the body can respond to diseases. This study was designed to investigate the protective actions of vitamin E (Vit-E) and lactobacillus plantarum (Lac-B) against mercuric chloride (HgCl
)-induced kidney injury. Thirty albino rats were divided into five groups: group 1 served as the normal group; rats in group 2 received high doses of HgCl
; rats in groups 3, 4 and 5 were given Vit-E, Lac-B and the combination of Vit-E and Lac-B, respectively along with HgCl
for two weeks. HgCl
provoked renal injury, manifested by elevation in serum urea, urea nitrogen and creatinine. Kidney levels of oxidative stress and inflammation were markedly increased post HgCl
administration. Moreover, HgCl
significantly elevated the gene expression levels of VCAM-1 and cystatin
, while podocin was downregulated. Additionally, it markedly decreased the protein expression of Beclin-1 and Bcl-2. Histopathological examination revealed massive degeneration with congested blood vessels following HgCl
administration. Treatment with Vit-E or/and Lac-B restored the normal levels of the previously mentioned parameters, as well as improved the morphology of kidney tissues. Both Vit-E and Lac-B provided a protective effect against HgCl
-induced kidney damage by regulating autophagy and apoptosis.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Bcl-2 protein</subject><subject>Beclin-1 - metabolism</subject><subject>Blood vessels</subject><subject>Creatinine</subject><subject>Cystatin C</subject><subject>Degeneration</subject><subject>Gene expression</subject><subject>Homeostasis</subject><subject>Intoxication</subject><subject>Kidney - metabolism</subject><subject>Kidneys</subject><subject>Lactobacilli</subject><subject>Lactobacillus plantarum - metabolism</subject><subject>Mercuric chloride</subject><subject>Mercuric Chloride - toxicity</subject><subject>Mercury compounds</subject><subject>Oxidative Stress</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Rats</subject><subject>Tocopherol</subject><subject>Urea - pharmacology</subject><subject>Ureas</subject><subject>Vascular cell adhesion molecule 1</subject><subject>Vitamin E</subject><subject>Vitamin E - metabolism</subject><subject>Vitamin E - pharmacology</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpVkUtLJDEUhYOMqKMu3Upg1uUkdeu5EXoaxxEaFVG3IZWkutNWJTV5jLS_3vgY0dW9cD_OuZyD0BElJwAt-anXo88hB1oCKbfQHi3yPCOkqr992nfRd-_XhCSwbHfQLlRF21ZA99DT3Fnvsxu1jAMP2hrcqfColMGzGOy04ssN5kbi2WSnYL32-MLIKJTE3Qbf68BHbfDZK7LgItiOCz0M0ePrgZvAXRxxWDkblyv8S4lBm4ziy-Rg3cMB2u754NXh-9xHd7_Pbud_ssXV-cV8tsgE1DRkgpcVlwL6QkFbq7aThcwLUvWKylq2UtRlJztSdUSW0OQpkxREDzQvSSNkU8E-On3TnWI3KimUCY4PbHJ65G7DLNfs68XoFVvaf6ytoSIASeDHu4Czf6Pyga1tdCb9zPK6aMqiSW6Jyt4o8ZKoU_2HAyXspSr2parEH39-64P-3w08A9k2kiI</recordid><startdate>20221204</startdate><enddate>20221204</enddate><creator>Alhusaini, Ahlam M</creator><creator>Alhumaidan, Sara A</creator><creator>Alharbi, Ghaida M</creator><creator>Alzahrani, Eman A</creator><creator>Sarawi, Wedad S</creator><creator>Alomar, Hatun A</creator><creator>Alanazi, Abeer M</creator><creator>Mattar, Dareen S</creator><creator>Hasan, Iman H</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7495-0592</orcidid><orcidid>https://orcid.org/0000-0003-2905-8882</orcidid><orcidid>https://orcid.org/0000-0001-6376-9464</orcidid><orcidid>https://orcid.org/0000-0001-7311-1412</orcidid></search><sort><creationdate>20221204</creationdate><title>Cross-Regulation between Autophagy and Apoptosis Induced by Vitamin E and Lactobacillus Plantarum through Beclin-1 Network</title><author>Alhusaini, Ahlam M ; 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This study was designed to investigate the protective actions of vitamin E (Vit-E) and lactobacillus plantarum (Lac-B) against mercuric chloride (HgCl
)-induced kidney injury. Thirty albino rats were divided into five groups: group 1 served as the normal group; rats in group 2 received high doses of HgCl
; rats in groups 3, 4 and 5 were given Vit-E, Lac-B and the combination of Vit-E and Lac-B, respectively along with HgCl
for two weeks. HgCl
provoked renal injury, manifested by elevation in serum urea, urea nitrogen and creatinine. Kidney levels of oxidative stress and inflammation were markedly increased post HgCl
administration. Moreover, HgCl
significantly elevated the gene expression levels of VCAM-1 and cystatin
, while podocin was downregulated. Additionally, it markedly decreased the protein expression of Beclin-1 and Bcl-2. Histopathological examination revealed massive degeneration with congested blood vessels following HgCl
administration. Treatment with Vit-E or/and Lac-B restored the normal levels of the previously mentioned parameters, as well as improved the morphology of kidney tissues. Both Vit-E and Lac-B provided a protective effect against HgCl
-induced kidney damage by regulating autophagy and apoptosis.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36499631</pmid><doi>10.3390/ijms232315305</doi><orcidid>https://orcid.org/0000-0001-7495-0592</orcidid><orcidid>https://orcid.org/0000-0003-2905-8882</orcidid><orcidid>https://orcid.org/0000-0001-6376-9464</orcidid><orcidid>https://orcid.org/0000-0001-7311-1412</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; MDPI - Multidisciplinary Digital Publishing Institute; PubMed Central |
| subjects | Animals Antioxidants Antioxidants - pharmacology Apoptosis Autophagy Bcl-2 protein Beclin-1 - metabolism Blood vessels Creatinine Cystatin C Degeneration Gene expression Homeostasis Intoxication Kidney - metabolism Kidneys Lactobacilli Lactobacillus plantarum - metabolism Mercuric chloride Mercuric Chloride - toxicity Mercury compounds Oxidative Stress Protein expression Proteins Rats Tocopherol Urea - pharmacology Ureas Vascular cell adhesion molecule 1 Vitamin E Vitamin E - metabolism Vitamin E - pharmacology |
| title | Cross-Regulation between Autophagy and Apoptosis Induced by Vitamin E and Lactobacillus Plantarum through Beclin-1 Network |
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