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Mechanistic Insights into Oxidative Stress and Apoptosis Mediated by Tannic Acid in Human Liver Hepatocellular Carcinoma Cells
The study investigated the cytotoxic effect of a natural polyphenolic compound Tannic acid (TA) on human liver hepatocellular carcinoma (HepG2) cells and elucidated the possible mechanisms that lead to apoptosis and oxidative stress HepG2 cell. The HepG2 cells were treated with TA for 24 h and vario...
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Published in: | International journal of molecular sciences 2019-12, Vol.20 (24), p.6145 |
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description | The study investigated the cytotoxic effect of a natural polyphenolic compound Tannic acid (TA) on human liver hepatocellular carcinoma (HepG2) cells and elucidated the possible mechanisms that lead to apoptosis and oxidative stress HepG2 cell. The HepG2 cells were treated with TA for 24 h and various assays were conducted to determine whether TA could induce cell death and oxidative stress. The cell viability assay was used to determine the half maximal inhibitory concentration (IC
), caspase activity and cellular ATP were determined by luminometry. Microscopy was employed to determine deoxyribonucleic acid (DNA) integrity, while thiobarbituric acid (TBARS) and nitric oxide synthase (NOS) assays were used to elucidate cellular reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively. Western blotting was used to confirm protein expression. The results revealed that tannic acid induced caspase activation and increased the presence of cellular ROS and RNS, while downregulating antioxidant expression. Tannic acid also showed increased cell death and increased DNA fragmentation. In conclusion, TA was able to induce apoptosis by DNA fragmentation via caspase-dependent and caspase-independent mechanism. It was also able to induce oxidative stress, consequently contributing to cell death. |
doi_str_mv | 10.3390/ijms20246145 |
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), caspase activity and cellular ATP were determined by luminometry. Microscopy was employed to determine deoxyribonucleic acid (DNA) integrity, while thiobarbituric acid (TBARS) and nitric oxide synthase (NOS) assays were used to elucidate cellular reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively. Western blotting was used to confirm protein expression. The results revealed that tannic acid induced caspase activation and increased the presence of cellular ROS and RNS, while downregulating antioxidant expression. Tannic acid also showed increased cell death and increased DNA fragmentation. In conclusion, TA was able to induce apoptosis by DNA fragmentation via caspase-dependent and caspase-independent mechanism. It was also able to induce oxidative stress, consequently contributing to cell death.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms20246145</identifier><identifier>PMID: 31817549</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acids ; Antioxidants ; Apoptosis ; Apoptosis - drug effects ; Assaying ; Cancer therapies ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Caspase ; Cell death ; Cell viability ; Chemotherapy ; Cytotoxicity ; Deoxyribonucleic acid ; DNA ; DNA fragmentation ; Fragmentation ; Gene Expression Regulation, Neoplastic - drug effects ; Hep G2 Cells ; Hepatocellular carcinoma ; Hepatocytes ; Humans ; Investigations ; Leukemia ; Liver ; Liver cancer ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Metabolism ; Mortality ; Neoplasm Proteins - biosynthesis ; Nitric oxide ; Nitric-oxide synthase ; Oxidative stress ; Oxidative Stress - drug effects ; Polyphenols ; Radiation ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Tannic acid ; Tannins - pharmacology ; Thiobarbituric acid ; Tumors ; Western blotting</subject><ispartof>International journal of molecular sciences, 2019-12, Vol.20 (24), p.6145</ispartof><rights>2019 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 (http://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>2019 by the authors. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-83314e8cba1f9a97b4dc06dafa3971dfac72685e056ed341d075bfa523ea9e173</citedby><cites>FETCH-LOGICAL-c412t-83314e8cba1f9a97b4dc06dafa3971dfac72685e056ed341d075bfa523ea9e173</cites><orcidid>0000-0003-3551-3458 ; 0000-0002-1085-7740</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2548669064/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2548669064?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,74998</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31817549$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mhlanga, Priscilla</creatorcontrib><creatorcontrib>Perumal, Pearl O</creatorcontrib><creatorcontrib>Somboro, Anou M</creatorcontrib><creatorcontrib>Amoako, Daniel G</creatorcontrib><creatorcontrib>Khumalo, Hezekiel M</creatorcontrib><creatorcontrib>Khan, Rene B</creatorcontrib><title>Mechanistic Insights into Oxidative Stress and Apoptosis Mediated by Tannic Acid in Human Liver Hepatocellular Carcinoma Cells</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>The study investigated the cytotoxic effect of a natural polyphenolic compound Tannic acid (TA) on human liver hepatocellular carcinoma (HepG2) cells and elucidated the possible mechanisms that lead to apoptosis and oxidative stress HepG2 cell. The HepG2 cells were treated with TA for 24 h and various assays were conducted to determine whether TA could induce cell death and oxidative stress. The cell viability assay was used to determine the half maximal inhibitory concentration (IC
), caspase activity and cellular ATP were determined by luminometry. Microscopy was employed to determine deoxyribonucleic acid (DNA) integrity, while thiobarbituric acid (TBARS) and nitric oxide synthase (NOS) assays were used to elucidate cellular reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively. Western blotting was used to confirm protein expression. The results revealed that tannic acid induced caspase activation and increased the presence of cellular ROS and RNS, while downregulating antioxidant expression. Tannic acid also showed increased cell death and increased DNA fragmentation. In conclusion, TA was able to induce apoptosis by DNA fragmentation via caspase-dependent and caspase-independent mechanism. It was also able to induce oxidative stress, consequently contributing to cell death.</description><subject>Acids</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Assaying</subject><subject>Cancer therapies</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Caspase</subject><subject>Cell death</subject><subject>Cell viability</subject><subject>Chemotherapy</subject><subject>Cytotoxicity</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA fragmentation</subject><subject>Fragmentation</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Hep G2 Cells</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatocytes</subject><subject>Humans</subject><subject>Investigations</subject><subject>Leukemia</subject><subject>Liver</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - 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drug effects</topic><topic>Assaying</topic><topic>Cancer therapies</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Caspase</topic><topic>Cell death</topic><topic>Cell viability</topic><topic>Chemotherapy</topic><topic>Cytotoxicity</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA fragmentation</topic><topic>Fragmentation</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Hep G2 Cells</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatocytes</topic><topic>Humans</topic><topic>Investigations</topic><topic>Leukemia</topic><topic>Liver</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>Metabolism</topic><topic>Mortality</topic><topic>Neoplasm Proteins - biosynthesis</topic><topic>Nitric oxide</topic><topic>Nitric-oxide synthase</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Polyphenols</topic><topic>Radiation</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Tannic acid</topic><topic>Tannins - pharmacology</topic><topic>Thiobarbituric acid</topic><topic>Tumors</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mhlanga, Priscilla</creatorcontrib><creatorcontrib>Perumal, Pearl O</creatorcontrib><creatorcontrib>Somboro, Anou M</creatorcontrib><creatorcontrib>Amoako, Daniel G</creatorcontrib><creatorcontrib>Khumalo, Hezekiel M</creatorcontrib><creatorcontrib>Khan, Rene B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</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>Medical Database (Alumni Edition)</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 Edition)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: 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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest research library</collection><collection>Research Library (Corporate)</collection><collection>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 Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mhlanga, Priscilla</au><au>Perumal, Pearl O</au><au>Somboro, Anou M</au><au>Amoako, Daniel G</au><au>Khumalo, Hezekiel M</au><au>Khan, Rene B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanistic Insights into Oxidative Stress and Apoptosis Mediated by Tannic Acid in Human Liver Hepatocellular Carcinoma Cells</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2019-12-05</date><risdate>2019</risdate><volume>20</volume><issue>24</issue><spage>6145</spage><pages>6145-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>The study investigated the cytotoxic effect of a natural polyphenolic compound Tannic acid (TA) on human liver hepatocellular carcinoma (HepG2) cells and elucidated the possible mechanisms that lead to apoptosis and oxidative stress HepG2 cell. The HepG2 cells were treated with TA for 24 h and various assays were conducted to determine whether TA could induce cell death and oxidative stress. The cell viability assay was used to determine the half maximal inhibitory concentration (IC
), caspase activity and cellular ATP were determined by luminometry. Microscopy was employed to determine deoxyribonucleic acid (DNA) integrity, while thiobarbituric acid (TBARS) and nitric oxide synthase (NOS) assays were used to elucidate cellular reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively. Western blotting was used to confirm protein expression. The results revealed that tannic acid induced caspase activation and increased the presence of cellular ROS and RNS, while downregulating antioxidant expression. Tannic acid also showed increased cell death and increased DNA fragmentation. In conclusion, TA was able to induce apoptosis by DNA fragmentation via caspase-dependent and caspase-independent mechanism. It was also able to induce oxidative stress, consequently contributing to cell death.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>31817549</pmid><doi>10.3390/ijms20246145</doi><orcidid>https://orcid.org/0000-0003-3551-3458</orcidid><orcidid>https://orcid.org/0000-0002-1085-7740</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Acids Antioxidants Apoptosis Apoptosis - drug effects Assaying Cancer therapies Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Caspase Cell death Cell viability Chemotherapy Cytotoxicity Deoxyribonucleic acid DNA DNA fragmentation Fragmentation Gene Expression Regulation, Neoplastic - drug effects Hep G2 Cells Hepatocellular carcinoma Hepatocytes Humans Investigations Leukemia Liver Liver cancer Liver Neoplasms - metabolism Liver Neoplasms - pathology Metabolism Mortality Neoplasm Proteins - biosynthesis Nitric oxide Nitric-oxide synthase Oxidative stress Oxidative Stress - drug effects Polyphenols Radiation Reactive oxygen species Reactive Oxygen Species - metabolism Tannic acid Tannins - pharmacology Thiobarbituric acid Tumors Western blotting |
title | Mechanistic Insights into Oxidative Stress and Apoptosis Mediated by Tannic Acid in Human Liver Hepatocellular Carcinoma Cells |
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