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5-O-Demethylnobiletin Alleviates CCl4-Induced Acute Liver Injury by Equilibrating ROS-Mediated Apoptosis and Autophagy Induction
Polymethoxyflavanoids (PMFs) have exhibited a vast array of therapeutic biological properties. 5-O-Demethylnobiletin (5-DN) is one such PMF having anti-inflammatory activity, yet its role in hepatoprotection has not been studied before. Results from in vitro study revealed that 5-DN did not exert a...
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Published in: | International journal of molecular sciences 2021-02, Vol.22 (3), p.1083 |
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description | Polymethoxyflavanoids (PMFs) have exhibited a vast array of therapeutic biological properties. 5-O-Demethylnobiletin (5-DN) is one such PMF having anti-inflammatory activity, yet its role in hepatoprotection has not been studied before. Results from in vitro study revealed that 5-DN did not exert a high level of cytotoxicity on HepG2 cells at 40 μM, and it was able to rescue HepG2 cell death induced by carbon tetrachloride (CCl4). Subsequently, we investigated acute liver injury on BALB/c mice induced by CCl4 through the intraperitoneal injection of 1 mL/kg CCl4 and co-administration of 5-DN at (1 and 2 mg/kg) by oral gavage for 15 days. The results illustrated that treatment with 5-DN attenuated CCl4-induced elevated serum aminotransferase (AST)/alanine aminotransferase (ALT) ratio and significantly ameliorated severe hepatic damage such as inflammation and fibrosis evidenced through lesser aberrations in the liver histology of 5-DN dose groups. Additionally, 5-DN efficiently counteracted and equilibrated the production of ROS accelerated by CCl4 and dramatically downregulated the expression of CYP2E1 vitally involved in converting CCl4 to toxic free radicals and also enhanced the antioxidant enzymes. 5-DN treatment also inhibited cell proliferation and inflammatory pathway abnormally regulated by CCl4 treatment. Furthermore, the apoptotic response induced by CCl4 treatment was remarkably reduced by enhanced Bcl-2 expression and noticeable reduction in Bax, Bid, cleaved caspase 3, caspase 9, and apaf-1 expression. 5-DN treatment also induced the conversion of LC3 and promoted the autophagic flux. Conclusively, 5-DN exhibited hepatoprotective effects in vitro and in vivo and prevented liver fibrosis induced by CCl4. |
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Results from in vitro study revealed that 5-DN did not exert a high level of cytotoxicity on HepG2 cells at 40 μM, and it was able to rescue HepG2 cell death induced by carbon tetrachloride (CCl4). Subsequently, we investigated acute liver injury on BALB/c mice induced by CCl4 through the intraperitoneal injection of 1 mL/kg CCl4 and co-administration of 5-DN at (1 and 2 mg/kg) by oral gavage for 15 days. The results illustrated that treatment with 5-DN attenuated CCl4-induced elevated serum aminotransferase (AST)/alanine aminotransferase (ALT) ratio and significantly ameliorated severe hepatic damage such as inflammation and fibrosis evidenced through lesser aberrations in the liver histology of 5-DN dose groups. Additionally, 5-DN efficiently counteracted and equilibrated the production of ROS accelerated by CCl4 and dramatically downregulated the expression of CYP2E1 vitally involved in converting CCl4 to toxic free radicals and also enhanced the antioxidant enzymes. 5-DN treatment also inhibited cell proliferation and inflammatory pathway abnormally regulated by CCl4 treatment. Furthermore, the apoptotic response induced by CCl4 treatment was remarkably reduced by enhanced Bcl-2 expression and noticeable reduction in Bax, Bid, cleaved caspase 3, caspase 9, and apaf-1 expression. 5-DN treatment also induced the conversion of LC3 and promoted the autophagic flux. Conclusively, 5-DN exhibited hepatoprotective effects in vitro and in vivo and prevented liver fibrosis induced by CCl4.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms22031083</identifier><identifier>PMID: 33499185</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>5-O-demethylnobiletin (5-DN) ; Alanine ; Alanine transaminase ; Anti-inflammatory agents ; Antioxidants ; Apaf-1 protein ; Apoptosis ; Autophagy ; Bcl-2 protein ; Biocompatibility ; Biological properties ; Carbon tetrachloride ; Caspase-3 ; Caspase-9 ; CCL4 protein ; Cell death ; Cell proliferation ; Citrus fruits ; Collagen ; cytochrome P450 ; Cytokines ; Cytotoxicity ; Endoplasmic reticulum ; Fibrosis ; Flavonoids ; Free radicals ; Hepatitis ; Histology ; Inflammation ; Kinases ; Lipid peroxidation ; Liver ; Liver cancer ; MAP kinase ; Morphology ; Oxidative stress ; Phagocytosis ; Proteins ; reactive oxygen species (ROS) ; Tumor necrosis factor-TNF</subject><ispartof>International journal of molecular sciences, 2021-02, Vol.22 (3), p.1083</ispartof><rights>2021. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-42646cb33f7b2d9cf0af92f492aa7ea73fe009fd313d6c9c04192274c558d3ee3</citedby><cites>FETCH-LOGICAL-c455t-42646cb33f7b2d9cf0af92f492aa7ea73fe009fd313d6c9c04192274c558d3ee3</cites><orcidid>0000-0001-6757-0241 ; 0000-0001-8391-8041</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2481398527/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2481398527?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,44590,53791,53793,75126</link.rule.ids></links><search><creatorcontrib>Chang, Sukkum Ngullie</creatorcontrib><creatorcontrib>Kim, Se Ho</creatorcontrib><creatorcontrib>Dey, Debasish Kumar</creatorcontrib><creatorcontrib>Park, Seon Min</creatorcontrib><creatorcontrib>Nasif, Omaima</creatorcontrib><creatorcontrib>Bajpai, Vivek K.</creatorcontrib><creatorcontrib>Kang, Sun Chul</creatorcontrib><creatorcontrib>Lee, Jintae</creatorcontrib><creatorcontrib>Park, Jae Gyu</creatorcontrib><title>5-O-Demethylnobiletin Alleviates CCl4-Induced Acute Liver Injury by Equilibrating ROS-Mediated Apoptosis and Autophagy Induction</title><title>International journal of molecular sciences</title><description>Polymethoxyflavanoids (PMFs) have exhibited a vast array of therapeutic biological properties. 5-O-Demethylnobiletin (5-DN) is one such PMF having anti-inflammatory activity, yet its role in hepatoprotection has not been studied before. Results from in vitro study revealed that 5-DN did not exert a high level of cytotoxicity on HepG2 cells at 40 μM, and it was able to rescue HepG2 cell death induced by carbon tetrachloride (CCl4). Subsequently, we investigated acute liver injury on BALB/c mice induced by CCl4 through the intraperitoneal injection of 1 mL/kg CCl4 and co-administration of 5-DN at (1 and 2 mg/kg) by oral gavage for 15 days. The results illustrated that treatment with 5-DN attenuated CCl4-induced elevated serum aminotransferase (AST)/alanine aminotransferase (ALT) ratio and significantly ameliorated severe hepatic damage such as inflammation and fibrosis evidenced through lesser aberrations in the liver histology of 5-DN dose groups. Additionally, 5-DN efficiently counteracted and equilibrated the production of ROS accelerated by CCl4 and dramatically downregulated the expression of CYP2E1 vitally involved in converting CCl4 to toxic free radicals and also enhanced the antioxidant enzymes. 5-DN treatment also inhibited cell proliferation and inflammatory pathway abnormally regulated by CCl4 treatment. Furthermore, the apoptotic response induced by CCl4 treatment was remarkably reduced by enhanced Bcl-2 expression and noticeable reduction in Bax, Bid, cleaved caspase 3, caspase 9, and apaf-1 expression. 5-DN treatment also induced the conversion of LC3 and promoted the autophagic flux. Conclusively, 5-DN exhibited hepatoprotective effects in vitro and in vivo and prevented liver fibrosis induced by CCl4.</description><subject>5-O-demethylnobiletin (5-DN)</subject><subject>Alanine</subject><subject>Alanine transaminase</subject><subject>Anti-inflammatory agents</subject><subject>Antioxidants</subject><subject>Apaf-1 protein</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Bcl-2 protein</subject><subject>Biocompatibility</subject><subject>Biological properties</subject><subject>Carbon tetrachloride</subject><subject>Caspase-3</subject><subject>Caspase-9</subject><subject>CCL4 protein</subject><subject>Cell death</subject><subject>Cell proliferation</subject><subject>Citrus fruits</subject><subject>Collagen</subject><subject>cytochrome P450</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Endoplasmic reticulum</subject><subject>Fibrosis</subject><subject>Flavonoids</subject><subject>Free radicals</subject><subject>Hepatitis</subject><subject>Histology</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Lipid peroxidation</subject><subject>Liver</subject><subject>Liver cancer</subject><subject>MAP kinase</subject><subject>Morphology</subject><subject>Oxidative stress</subject><subject>Phagocytosis</subject><subject>Proteins</subject><subject>reactive oxygen species (ROS)</subject><subject>Tumor necrosis factor-TNF</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpVkctq3DAUhk1padK0uz6AoNs6lXWxrU1hmKTpwJSBXtZClo9mZDSWI8kD3vXRq2RCSVbn-n8_h1MUHyt8TanAX-xwjIRgWuGWviouK0ZIiXHdvH6WXxTvYhwwJpRw8ba4oJQJUbX8svjLy115A0dIh8WNvrMOkh3Ryjk4WZUgovXasXIz9rOGHq30nABt7QkC2ozDHBbULej2frbOdkFl6R793P0qf0D_oM6CyU_JRxuRGnM1Jz8d1H5Bj8Bk_fi-eGOUi_DhKV4Vf77d_l5_L7e7u816tS014zyVjNSs1h2lpulIL7TByghimCBKNaAaagBjYXpa0b7WQmNWCUIapjlvewpAr4rNmdt7Ncgp2KMKi_TKyseGD3upQrLagcSCg-hMtjOGccG67MN5VQPFDcFGZ9bXM2uauyP0GsYUlHsBfTkZ7UHu_Uk2bc0JFRnw6QkQ_P0MMcnBz2HM90vC2oqKlpMmb30-b-ngYwxg_jtUWD78Xj7_Pf0H2eGiVA</recordid><startdate>20210201</startdate><enddate>20210201</enddate><creator>Chang, Sukkum Ngullie</creator><creator>Kim, Se Ho</creator><creator>Dey, Debasish Kumar</creator><creator>Park, Seon Min</creator><creator>Nasif, Omaima</creator><creator>Bajpai, Vivek K.</creator><creator>Kang, Sun Chul</creator><creator>Lee, Jintae</creator><creator>Park, Jae Gyu</creator><general>MDPI AG</general><general>MDPI</general><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><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-6757-0241</orcidid><orcidid>https://orcid.org/0000-0001-8391-8041</orcidid></search><sort><creationdate>20210201</creationdate><title>5-O-Demethylnobiletin Alleviates CCl4-Induced Acute Liver Injury by Equilibrating ROS-Mediated Apoptosis and Autophagy Induction</title><author>Chang, Sukkum Ngullie ; 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Results from in vitro study revealed that 5-DN did not exert a high level of cytotoxicity on HepG2 cells at 40 μM, and it was able to rescue HepG2 cell death induced by carbon tetrachloride (CCl4). Subsequently, we investigated acute liver injury on BALB/c mice induced by CCl4 through the intraperitoneal injection of 1 mL/kg CCl4 and co-administration of 5-DN at (1 and 2 mg/kg) by oral gavage for 15 days. The results illustrated that treatment with 5-DN attenuated CCl4-induced elevated serum aminotransferase (AST)/alanine aminotransferase (ALT) ratio and significantly ameliorated severe hepatic damage such as inflammation and fibrosis evidenced through lesser aberrations in the liver histology of 5-DN dose groups. Additionally, 5-DN efficiently counteracted and equilibrated the production of ROS accelerated by CCl4 and dramatically downregulated the expression of CYP2E1 vitally involved in converting CCl4 to toxic free radicals and also enhanced the antioxidant enzymes. 5-DN treatment also inhibited cell proliferation and inflammatory pathway abnormally regulated by CCl4 treatment. Furthermore, the apoptotic response induced by CCl4 treatment was remarkably reduced by enhanced Bcl-2 expression and noticeable reduction in Bax, Bid, cleaved caspase 3, caspase 9, and apaf-1 expression. 5-DN treatment also induced the conversion of LC3 and promoted the autophagic flux. 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subjects | 5-O-demethylnobiletin (5-DN) Alanine Alanine transaminase Anti-inflammatory agents Antioxidants Apaf-1 protein Apoptosis Autophagy Bcl-2 protein Biocompatibility Biological properties Carbon tetrachloride Caspase-3 Caspase-9 CCL4 protein Cell death Cell proliferation Citrus fruits Collagen cytochrome P450 Cytokines Cytotoxicity Endoplasmic reticulum Fibrosis Flavonoids Free radicals Hepatitis Histology Inflammation Kinases Lipid peroxidation Liver Liver cancer MAP kinase Morphology Oxidative stress Phagocytosis Proteins reactive oxygen species (ROS) Tumor necrosis factor-TNF |
title | 5-O-Demethylnobiletin Alleviates CCl4-Induced Acute Liver Injury by Equilibrating ROS-Mediated Apoptosis and Autophagy Induction |
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