Hepatoprotective Effects of (−) Epicatechin in CCl4-Induced Toxicity Model Are Mediated via Modulation of Oxidative Stress Markers in Rats
Objective. (−) Epicatechin (EP) is a naturally occurring antioxidant flavonoid found in some green plants. The current study was designed to evaluate the potential role of antioxidant mechanisms in the hepatoprotective properties of EP using the carbon tetrachloride (CCl4)-induced acute liver injury...
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| Veröffentlicht in: | Evidence-based complementary and alternative medicine 2021-12, Vol.2021, p.1-12 |
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| creator | Alkinani, Khadijah B. Ali, Ehab M. M. Al-Shaikh, Turki M. Awlia Khan, Jalaluddin A. Al-naomasi, Tahani M. Ali, Soad S. Abduljawad, Asaad A. Mosa, Osama F. Zafar, Tariq A. |
| description | Objective. (−) Epicatechin (EP) is a naturally occurring antioxidant flavonoid found in some green plants. The current study was designed to evaluate the potential role of antioxidant mechanisms in the hepatoprotective properties of EP using the carbon tetrachloride (CCl4)-induced acute liver injury model. Materials and Methods. Rats (n = 7 per group) were divided into five groups including control group, (−) epicatechin group (20 mg·kg−1 body weight), CCl4 group (1 mL−1 body weight), CCl4-EP treatment group, and CCl4-silymarin (SILY) group. The levels of enzymes including hepatic malondialdehyde (MDA), glutathione (GSH), catalase (CAT), glutathione S-transferase (GST), nitric oxide synthase (NOS), glutathione peroxidase (GPx), and cytochrome P450 (CYP450) were analyzed via enzyme-linked immunosorbent assay (ELISA). Histological studies were performed on all groups to assess the regenerative effects of test sample and compare it with the control group. Results. Test compound EP and standard drug silymarin (SILY) considerably reduced liver function enzyme levels in the blood, which were raised by CCl4 administration, and increased serum albumin and total protein (TP) concentrations. The hepatic malondialdehyde (MDA) level was considerably declined, whereas glutathione (GSH), catalase (CAT), glutathione S-transferase (GST), nitric oxide synthase (NOS), glutathione peroxidase (GPx), and cytochrome P450 (CYP450) levels were upregulated in the EC-treated groups. The hepatoprotective results of the study were further confirmed via the histological assessments, which indicated a regeneration of the damaged hepatic tissue in treated rats. Conclusions. The results of this study revealed a significant protective efficacy of EP against CCl4-induced liver injury, which was potentially mediated via upregulation of antioxidant enzymes and direct scavenging effects of the compound against free radicals. |
| doi_str_mv | 10.1155/2021/4655150 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8716200</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2615861835</sourcerecordid><originalsourceid>FETCH-LOGICAL-c425t-a301f05dc5733aac07c99d8e051bad520a4718618efa7eeefa60bcf456d18ca73</originalsourceid><addsrcrecordid>eNp9kc1q3DAUhUVpaX7aXR9A0E1K40SyLcveFMIw-YEMgTaF7sQd6bpR6rEcSZ4mb9BFV33EPknlzBBoFwVxdbn34-iIQ8gbzo44F-I4Zzk_LishuGDPyC6XJc_KvK6fP_Xyyw7ZC-GWsbyRUr4kO0XZyIo1xS75eY4DRDd4F1FHu0Y6b9vUBepaevD7x693dD5YDWl7Y3uazmzWldlFb0aNhl67e6ttfKALZ7CjJx7pAo1NuKFrC9N47CBa1096V_fWwOMjn6LHEOgC_Df0YZL9CDG8Ii9a6AK-3t775PPp_Hp2nl1enV3MTi4zXeYiZlAw3jJhtJBFAaCZ1E1jamSCL8GInEEpeV3xGluQiKlWbKnbUlSG1xpksU8-bHSHcblCo7GPHjo1eLsC_6AcWPX3prc36qtbq1ryKmcsCRxsBby7GzFEtbJBY9dBj24MKq8SVycPdULf_oPeutH36XsTJSabhUjU4YbS3oXgsX0yw5maYlZTzGobc8Lfb_CUiYHv9v_0H3SWqAg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2615861835</pqid></control><display><type>article</type><title>Hepatoprotective Effects of (−) Epicatechin in CCl4-Induced Toxicity Model Are Mediated via Modulation of Oxidative Stress Markers in Rats</title><source>Wiley Online Library Open Access</source><source>PubMed Central(OpenAccess)</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><source>PubMed Central Open Access</source><creator>Alkinani, Khadijah B. ; Ali, Ehab M. M. ; Al-Shaikh, Turki M. ; Awlia Khan, Jalaluddin A. ; Al-naomasi, Tahani M. ; Ali, Soad S. ; Abduljawad, Asaad A. ; Mosa, Osama F. ; Zafar, Tariq A.</creator><contributor>Garg, Ruchika ; Ruchika Garg</contributor><creatorcontrib>Alkinani, Khadijah B. ; Ali, Ehab M. M. ; Al-Shaikh, Turki M. ; Awlia Khan, Jalaluddin A. ; Al-naomasi, Tahani M. ; Ali, Soad S. ; Abduljawad, Asaad A. ; Mosa, Osama F. ; Zafar, Tariq A. ; Garg, Ruchika ; Ruchika Garg</creatorcontrib><description>Objective. (−) Epicatechin (EP) is a naturally occurring antioxidant flavonoid found in some green plants. The current study was designed to evaluate the potential role of antioxidant mechanisms in the hepatoprotective properties of EP using the carbon tetrachloride (CCl4)-induced acute liver injury model. Materials and Methods. Rats (n = 7 per group) were divided into five groups including control group, (−) epicatechin group (20 mg·kg−1 body weight), CCl4 group (1 mL−1 body weight), CCl4-EP treatment group, and CCl4-silymarin (SILY) group. The levels of enzymes including hepatic malondialdehyde (MDA), glutathione (GSH), catalase (CAT), glutathione S-transferase (GST), nitric oxide synthase (NOS), glutathione peroxidase (GPx), and cytochrome P450 (CYP450) were analyzed via enzyme-linked immunosorbent assay (ELISA). Histological studies were performed on all groups to assess the regenerative effects of test sample and compare it with the control group. Results. Test compound EP and standard drug silymarin (SILY) considerably reduced liver function enzyme levels in the blood, which were raised by CCl4 administration, and increased serum albumin and total protein (TP) concentrations. The hepatic malondialdehyde (MDA) level was considerably declined, whereas glutathione (GSH), catalase (CAT), glutathione S-transferase (GST), nitric oxide synthase (NOS), glutathione peroxidase (GPx), and cytochrome P450 (CYP450) levels were upregulated in the EC-treated groups. The hepatoprotective results of the study were further confirmed via the histological assessments, which indicated a regeneration of the damaged hepatic tissue in treated rats. Conclusions. The results of this study revealed a significant protective efficacy of EP against CCl4-induced liver injury, which was potentially mediated via upregulation of antioxidant enzymes and direct scavenging effects of the compound against free radicals.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2021/4655150</identifier><identifier>PMID: 34976093</identifier><language>eng</language><publisher>New York: Hindawi</publisher><subject>Antioxidants ; Body weight ; Carbon tetrachloride ; Catalase ; Cytochrome P450 ; Disease ; Enzyme-linked immunosorbent assay ; Enzymes ; Epicatechin ; Flavonoids ; Free radicals ; Glutathione peroxidase ; Glutathione transferase ; Hydrogen peroxide ; Liver ; Malondialdehyde ; Nitric-oxide synthase ; Oxidation ; Oxidative stress ; Polyphenols ; Proteins ; Silymarin ; Toxicity ; Tumor necrosis factor-TNF</subject><ispartof>Evidence-based complementary and alternative medicine, 2021-12, Vol.2021, p.1-12</ispartof><rights>Copyright © 2021 Khadijah B. Alkinani et al.</rights><rights>Copyright © 2021 Khadijah B. Alkinani et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 Khadijah B. Alkinani et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-a301f05dc5733aac07c99d8e051bad520a4718618efa7eeefa60bcf456d18ca73</citedby><cites>FETCH-LOGICAL-c425t-a301f05dc5733aac07c99d8e051bad520a4718618efa7eeefa60bcf456d18ca73</cites><orcidid>0000-0002-2434-2027 ; 0000-0001-5052-7116 ; 0000-0003-4895-9803 ; 0000-0002-4469-8581 ; 0000-0002-2475-0645 ; 0000-0001-5585-8520 ; 0000-0002-1894-5382 ; 0000-0003-2319-4023 ; 0000-0001-5866-5177</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/PMC8716200/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8716200/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids></links><search><contributor>Garg, Ruchika</contributor><contributor>Ruchika Garg</contributor><creatorcontrib>Alkinani, Khadijah B.</creatorcontrib><creatorcontrib>Ali, Ehab M. M.</creatorcontrib><creatorcontrib>Al-Shaikh, Turki M.</creatorcontrib><creatorcontrib>Awlia Khan, Jalaluddin A.</creatorcontrib><creatorcontrib>Al-naomasi, Tahani M.</creatorcontrib><creatorcontrib>Ali, Soad S.</creatorcontrib><creatorcontrib>Abduljawad, Asaad A.</creatorcontrib><creatorcontrib>Mosa, Osama F.</creatorcontrib><creatorcontrib>Zafar, Tariq A.</creatorcontrib><title>Hepatoprotective Effects of (−) Epicatechin in CCl4-Induced Toxicity Model Are Mediated via Modulation of Oxidative Stress Markers in Rats</title><title>Evidence-based complementary and alternative medicine</title><description>Objective. (−) Epicatechin (EP) is a naturally occurring antioxidant flavonoid found in some green plants. The current study was designed to evaluate the potential role of antioxidant mechanisms in the hepatoprotective properties of EP using the carbon tetrachloride (CCl4)-induced acute liver injury model. Materials and Methods. Rats (n = 7 per group) were divided into five groups including control group, (−) epicatechin group (20 mg·kg−1 body weight), CCl4 group (1 mL−1 body weight), CCl4-EP treatment group, and CCl4-silymarin (SILY) group. The levels of enzymes including hepatic malondialdehyde (MDA), glutathione (GSH), catalase (CAT), glutathione S-transferase (GST), nitric oxide synthase (NOS), glutathione peroxidase (GPx), and cytochrome P450 (CYP450) were analyzed via enzyme-linked immunosorbent assay (ELISA). Histological studies were performed on all groups to assess the regenerative effects of test sample and compare it with the control group. Results. Test compound EP and standard drug silymarin (SILY) considerably reduced liver function enzyme levels in the blood, which were raised by CCl4 administration, and increased serum albumin and total protein (TP) concentrations. The hepatic malondialdehyde (MDA) level was considerably declined, whereas glutathione (GSH), catalase (CAT), glutathione S-transferase (GST), nitric oxide synthase (NOS), glutathione peroxidase (GPx), and cytochrome P450 (CYP450) levels were upregulated in the EC-treated groups. The hepatoprotective results of the study were further confirmed via the histological assessments, which indicated a regeneration of the damaged hepatic tissue in treated rats. Conclusions. The results of this study revealed a significant protective efficacy of EP against CCl4-induced liver injury, which was potentially mediated via upregulation of antioxidant enzymes and direct scavenging effects of the compound against free radicals.</description><subject>Antioxidants</subject><subject>Body weight</subject><subject>Carbon tetrachloride</subject><subject>Catalase</subject><subject>Cytochrome P450</subject><subject>Disease</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Enzymes</subject><subject>Epicatechin</subject><subject>Flavonoids</subject><subject>Free radicals</subject><subject>Glutathione peroxidase</subject><subject>Glutathione transferase</subject><subject>Hydrogen peroxide</subject><subject>Liver</subject><subject>Malondialdehyde</subject><subject>Nitric-oxide synthase</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Polyphenols</subject><subject>Proteins</subject><subject>Silymarin</subject><subject>Toxicity</subject><subject>Tumor necrosis factor-TNF</subject><issn>1741-427X</issn><issn>1741-4288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>RHX</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>eNp9kc1q3DAUhUVpaX7aXR9A0E1K40SyLcveFMIw-YEMgTaF7sQd6bpR6rEcSZ4mb9BFV33EPknlzBBoFwVxdbn34-iIQ8gbzo44F-I4Zzk_LishuGDPyC6XJc_KvK6fP_Xyyw7ZC-GWsbyRUr4kO0XZyIo1xS75eY4DRDd4F1FHu0Y6b9vUBepaevD7x693dD5YDWl7Y3uazmzWldlFb0aNhl67e6ttfKALZ7CjJx7pAo1NuKFrC9N47CBa1096V_fWwOMjn6LHEOgC_Df0YZL9CDG8Ii9a6AK-3t775PPp_Hp2nl1enV3MTi4zXeYiZlAw3jJhtJBFAaCZ1E1jamSCL8GInEEpeV3xGluQiKlWbKnbUlSG1xpksU8-bHSHcblCo7GPHjo1eLsC_6AcWPX3prc36qtbq1ryKmcsCRxsBby7GzFEtbJBY9dBj24MKq8SVycPdULf_oPeutH36XsTJSabhUjU4YbS3oXgsX0yw5maYlZTzGobc8Lfb_CUiYHv9v_0H3SWqAg</recordid><startdate>20211222</startdate><enddate>20211222</enddate><creator>Alkinani, Khadijah B.</creator><creator>Ali, Ehab M. 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M. ; Al-Shaikh, Turki M. ; Awlia Khan, Jalaluddin A. ; Al-naomasi, Tahani M. ; Ali, Soad S. ; Abduljawad, Asaad A. ; Mosa, Osama F. ; Zafar, Tariq A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c425t-a301f05dc5733aac07c99d8e051bad520a4718618efa7eeefa60bcf456d18ca73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antioxidants</topic><topic>Body weight</topic><topic>Carbon tetrachloride</topic><topic>Catalase</topic><topic>Cytochrome P450</topic><topic>Disease</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Enzymes</topic><topic>Epicatechin</topic><topic>Flavonoids</topic><topic>Free radicals</topic><topic>Glutathione peroxidase</topic><topic>Glutathione transferase</topic><topic>Hydrogen peroxide</topic><topic>Liver</topic><topic>Malondialdehyde</topic><topic>Nitric-oxide synthase</topic><topic>Oxidation</topic><topic>Oxidative stress</topic><topic>Polyphenols</topic><topic>Proteins</topic><topic>Silymarin</topic><topic>Toxicity</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alkinani, Khadijah B.</creatorcontrib><creatorcontrib>Ali, Ehab M. M.</creatorcontrib><creatorcontrib>Al-Shaikh, Turki M.</creatorcontrib><creatorcontrib>Awlia Khan, Jalaluddin A.</creatorcontrib><creatorcontrib>Al-naomasi, Tahani M.</creatorcontrib><creatorcontrib>Ali, Soad S.</creatorcontrib><creatorcontrib>Abduljawad, Asaad A.</creatorcontrib><creatorcontrib>Mosa, Osama F.</creatorcontrib><creatorcontrib>Zafar, Tariq A.</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest - Health & Medical Complete保健、医学与药学数据库</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest Psychology Journals</collection><collection>ProQuest Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest Publicly Available Content database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Evidence-based complementary and alternative medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alkinani, Khadijah B.</au><au>Ali, Ehab M. M.</au><au>Al-Shaikh, Turki M.</au><au>Awlia Khan, Jalaluddin A.</au><au>Al-naomasi, Tahani M.</au><au>Ali, Soad S.</au><au>Abduljawad, Asaad A.</au><au>Mosa, Osama F.</au><au>Zafar, Tariq A.</au><au>Garg, Ruchika</au><au>Ruchika Garg</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatoprotective Effects of (−) Epicatechin in CCl4-Induced Toxicity Model Are Mediated via Modulation of Oxidative Stress Markers in Rats</atitle><jtitle>Evidence-based complementary and alternative medicine</jtitle><date>2021-12-22</date><risdate>2021</risdate><volume>2021</volume><spage>1</spage><epage>12</epage><pages>1-12</pages><issn>1741-427X</issn><eissn>1741-4288</eissn><abstract>Objective. (−) Epicatechin (EP) is a naturally occurring antioxidant flavonoid found in some green plants. The current study was designed to evaluate the potential role of antioxidant mechanisms in the hepatoprotective properties of EP using the carbon tetrachloride (CCl4)-induced acute liver injury model. Materials and Methods. Rats (n = 7 per group) were divided into five groups including control group, (−) epicatechin group (20 mg·kg−1 body weight), CCl4 group (1 mL−1 body weight), CCl4-EP treatment group, and CCl4-silymarin (SILY) group. The levels of enzymes including hepatic malondialdehyde (MDA), glutathione (GSH), catalase (CAT), glutathione S-transferase (GST), nitric oxide synthase (NOS), glutathione peroxidase (GPx), and cytochrome P450 (CYP450) were analyzed via enzyme-linked immunosorbent assay (ELISA). Histological studies were performed on all groups to assess the regenerative effects of test sample and compare it with the control group. Results. Test compound EP and standard drug silymarin (SILY) considerably reduced liver function enzyme levels in the blood, which were raised by CCl4 administration, and increased serum albumin and total protein (TP) concentrations. The hepatic malondialdehyde (MDA) level was considerably declined, whereas glutathione (GSH), catalase (CAT), glutathione S-transferase (GST), nitric oxide synthase (NOS), glutathione peroxidase (GPx), and cytochrome P450 (CYP450) levels were upregulated in the EC-treated groups. The hepatoprotective results of the study were further confirmed via the histological assessments, which indicated a regeneration of the damaged hepatic tissue in treated rats. Conclusions. The results of this study revealed a significant protective efficacy of EP against CCl4-induced liver injury, which was potentially mediated via upregulation of antioxidant enzymes and direct scavenging effects of the compound against free radicals.</abstract><cop>New York</cop><pub>Hindawi</pub><pmid>34976093</pmid><doi>10.1155/2021/4655150</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-2434-2027</orcidid><orcidid>https://orcid.org/0000-0001-5052-7116</orcidid><orcidid>https://orcid.org/0000-0003-4895-9803</orcidid><orcidid>https://orcid.org/0000-0002-4469-8581</orcidid><orcidid>https://orcid.org/0000-0002-2475-0645</orcidid><orcidid>https://orcid.org/0000-0001-5585-8520</orcidid><orcidid>https://orcid.org/0000-0002-1894-5382</orcidid><orcidid>https://orcid.org/0000-0003-2319-4023</orcidid><orcidid>https://orcid.org/0000-0001-5866-5177</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antioxidants Body weight Carbon tetrachloride Catalase Cytochrome P450 Disease Enzyme-linked immunosorbent assay Enzymes Epicatechin Flavonoids Free radicals Glutathione peroxidase Glutathione transferase Hydrogen peroxide Liver Malondialdehyde Nitric-oxide synthase Oxidation Oxidative stress Polyphenols Proteins Silymarin Toxicity Tumor necrosis factor-TNF |
| title | Hepatoprotective Effects of (−) Epicatechin in CCl4-Induced Toxicity Model Are Mediated via Modulation of Oxidative Stress Markers in Rats |
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