Ischemic insult induced apoptotic changes in PC12 cells: Protection by trans resveratrol
In this study, we determined the protective potential of trans resveratrol against oxygen–glucose deprivation (OGD) induced reactive oxygen species mediated apoptotic damages in PC12 cells. In vitro model of ischemic cerebral stroke was created by keeping cells in an OGD condition for 6 h followed b...
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| Veröffentlicht in: | European journal of pharmacology 2011-09, Vol.666 (1), p.5-11 |
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| creator | Agrawal, Megha Kumar, Vivek Kashyap, Mahendra P. Khanna, Vinay K. Randhawa, Gursharn S. Pant, Aditya B. |
| description | In this study, we determined the protective potential of
trans resveratrol against oxygen–glucose deprivation (OGD) induced reactive oxygen species mediated apoptotic damages in PC12 cells. In vitro model of ischemic cerebral stroke was created by keeping cells in an OGD condition for 6
h followed by 24
h reoxygenation. Cells received biologically safe doses (5, 10, and 25
μM) of
trans resveratrol in the following schedules for 24
h prior to OGD; during 6
h of OGD; for 24
h post OGD and whole treatment group which starts from 24
h before OGD and lasted to 24
h post OGD. Anti-ischemic potential of
trans resveratrol was assessed by measuring the regulation of lipid peroxidation, reactive oxygen species production, glutathione content, and expression (mRNA and protein) of apoptotic markers such as Bax, Bcl
2 and Caspase-3. Hypoxia inducible factor-1α (HIF-1α) was also assessed to correlate the changes with ischemic injuries. Significant (P
<
0.05) restoration in lipid peroxidation, reactive oxygen species, and glutathione content were observed following the treatment of
trans resveratrol in cells receiving OGD and re-oxygenation. Changes induced by
trans resveratrol could be correlated well with alterations in the expression of Bax, Bcl
2, Caspase-3 and HIF-1α. These results indicate that
trans resveratrol administration attenuates free radical formation and mitochondria mediated apoptosis perhaps by regulating the expressions of Bax, Bcl
2, and Caspase-3 in PC12 cells receiving OGD and re-oxygenation insult.
[Display omitted] |
| doi_str_mv | 10.1016/j.ejphar.2011.05.015 |
| format | Article |
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trans resveratrol against oxygen–glucose deprivation (OGD) induced reactive oxygen species mediated apoptotic damages in PC12 cells. In vitro model of ischemic cerebral stroke was created by keeping cells in an OGD condition for 6
h followed by 24
h reoxygenation. Cells received biologically safe doses (5, 10, and 25
μM) of
trans resveratrol in the following schedules for 24
h prior to OGD; during 6
h of OGD; for 24
h post OGD and whole treatment group which starts from 24
h before OGD and lasted to 24
h post OGD. Anti-ischemic potential of
trans resveratrol was assessed by measuring the regulation of lipid peroxidation, reactive oxygen species production, glutathione content, and expression (mRNA and protein) of apoptotic markers such as Bax, Bcl
2 and Caspase-3. Hypoxia inducible factor-1α (HIF-1α) was also assessed to correlate the changes with ischemic injuries. Significant (P
<
0.05) restoration in lipid peroxidation, reactive oxygen species, and glutathione content were observed following the treatment of
trans resveratrol in cells receiving OGD and re-oxygenation. Changes induced by
trans resveratrol could be correlated well with alterations in the expression of Bax, Bcl
2, Caspase-3 and HIF-1α. These results indicate that
trans resveratrol administration attenuates free radical formation and mitochondria mediated apoptosis perhaps by regulating the expressions of Bax, Bcl
2, and Caspase-3 in PC12 cells receiving OGD and re-oxygenation insult.
[Display omitted]</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2011.05.015</identifier><identifier>PMID: 21620820</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Animals ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; bcl-2-Associated X Protein - biosynthesis ; bcl-2-Associated X Protein - genetics ; Biological and medical sciences ; Brain Ischemia - genetics ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Brain Ischemia - prevention & control ; Caspase 3 - biosynthesis ; Caspase 3 - genetics ; Glucose - metabolism ; Glutathione - metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis ; Hypoxia-Inducible Factor 1, alpha Subunit - genetics ; Lipid Peroxidation - drug effects ; Medical sciences ; Neurons - drug effects ; Neurons - metabolism ; Neurons - pathology ; Neuroprotection ; Neuroprotective Agents - pharmacology ; OGD ; Oxidative Stress - drug effects ; Oxidative Stress - genetics ; Oxygen - metabolism ; PC12 cell ; PC12 Cells ; Pharmacology. Drug treatments ; Proto-Oncogene Proteins c-bcl-2 - biosynthesis ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Rats ; Reactive Oxygen Species - metabolism ; Stilbenes - pharmacology ; Trans resveratrol ; Transcription, Genetic - drug effects</subject><ispartof>European journal of pharmacology, 2011-09, Vol.666 (1), p.5-11</ispartof><rights>2011 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c457t-eb0173bf0d99f606903654ffb63fd9722287435b76149fbbf069cd86ea21c0f43</citedby><cites>FETCH-LOGICAL-c457t-eb0173bf0d99f606903654ffb63fd9722287435b76149fbbf069cd86ea21c0f43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014299911005450$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24306895$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21620820$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Agrawal, Megha</creatorcontrib><creatorcontrib>Kumar, Vivek</creatorcontrib><creatorcontrib>Kashyap, Mahendra P.</creatorcontrib><creatorcontrib>Khanna, Vinay K.</creatorcontrib><creatorcontrib>Randhawa, Gursharn S.</creatorcontrib><creatorcontrib>Pant, Aditya B.</creatorcontrib><title>Ischemic insult induced apoptotic changes in PC12 cells: Protection by trans resveratrol</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>In this study, we determined the protective potential of
trans resveratrol against oxygen–glucose deprivation (OGD) induced reactive oxygen species mediated apoptotic damages in PC12 cells. In vitro model of ischemic cerebral stroke was created by keeping cells in an OGD condition for 6
h followed by 24
h reoxygenation. Cells received biologically safe doses (5, 10, and 25
μM) of
trans resveratrol in the following schedules for 24
h prior to OGD; during 6
h of OGD; for 24
h post OGD and whole treatment group which starts from 24
h before OGD and lasted to 24
h post OGD. Anti-ischemic potential of
trans resveratrol was assessed by measuring the regulation of lipid peroxidation, reactive oxygen species production, glutathione content, and expression (mRNA and protein) of apoptotic markers such as Bax, Bcl
2 and Caspase-3. Hypoxia inducible factor-1α (HIF-1α) was also assessed to correlate the changes with ischemic injuries. Significant (P
<
0.05) restoration in lipid peroxidation, reactive oxygen species, and glutathione content were observed following the treatment of
trans resveratrol in cells receiving OGD and re-oxygenation. Changes induced by
trans resveratrol could be correlated well with alterations in the expression of Bax, Bcl
2, Caspase-3 and HIF-1α. These results indicate that
trans resveratrol administration attenuates free radical formation and mitochondria mediated apoptosis perhaps by regulating the expressions of Bax, Bcl
2, and Caspase-3 in PC12 cells receiving OGD and re-oxygenation insult.
[Display omitted]</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>bcl-2-Associated X Protein - biosynthesis</subject><subject>bcl-2-Associated X Protein - genetics</subject><subject>Biological and medical sciences</subject><subject>Brain Ischemia - genetics</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Brain Ischemia - prevention & control</subject><subject>Caspase 3 - biosynthesis</subject><subject>Caspase 3 - genetics</subject><subject>Glucose - metabolism</subject><subject>Glutathione - metabolism</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Medical sciences</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>OGD</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - genetics</subject><subject>Oxygen - metabolism</subject><subject>PC12 cell</subject><subject>PC12 Cells</subject><subject>Pharmacology. Drug treatments</subject><subject>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Rats</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Stilbenes - pharmacology</subject><subject>Trans resveratrol</subject><subject>Transcription, Genetic - drug effects</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFq3DAQhkVpabZJ3yAUX0pPdkeyJVs5BMqStIFAc0igNyHLo6wWr-VIciBvHy27TW89zWG-_5_hI-ScQkWBiu_bCrfzRoeKAaUV8Aoof0dWtGtlCS1l78kKgDYlk1KekE8xbgGAS8Y_khNGBYOOwYr8uYlmgztnCjfFZUx5DIvBodCzn5NPeWE2enrEmDfF3ZqywuA4xoviLviEJjk_Ff1LkYKeYhEwPmPQKfjxjHyweoz4-ThPycP11f36V3n7--fN-sdtaRrephJ7oG3dWxiktAKEhFrwxtpe1HaQLWOsa5ua962gjbR9BoU0QydQM2rANvUp-XbonYN_WjAmtXNx_6Ke0C9R5XgnWy5EJpsDaYKPMaBVc3A7HV4UBbVXqrbqoFTtlSrgKivNsS_HA0u_w-Et9NdhBr4eAR2NHm02YVz8xzU1iE7uiy4PHGYdzw6DisbhlGW7kEWqwbv_f_IKYhmWDA</recordid><startdate>20110901</startdate><enddate>20110901</enddate><creator>Agrawal, Megha</creator><creator>Kumar, Vivek</creator><creator>Kashyap, Mahendra P.</creator><creator>Khanna, Vinay K.</creator><creator>Randhawa, Gursharn S.</creator><creator>Pant, Aditya B.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20110901</creationdate><title>Ischemic insult induced apoptotic changes in PC12 cells: Protection by trans resveratrol</title><author>Agrawal, Megha ; Kumar, Vivek ; Kashyap, Mahendra P. ; Khanna, Vinay K. ; Randhawa, Gursharn S. ; Pant, Aditya B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c457t-eb0173bf0d99f606903654ffb63fd9722287435b76149fbbf069cd86ea21c0f43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>bcl-2-Associated X Protein - biosynthesis</topic><topic>bcl-2-Associated X Protein - genetics</topic><topic>Biological and medical sciences</topic><topic>Brain Ischemia - genetics</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Brain Ischemia - prevention & control</topic><topic>Caspase 3 - biosynthesis</topic><topic>Caspase 3 - genetics</topic><topic>Glucose - metabolism</topic><topic>Glutathione - metabolism</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Medical sciences</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>OGD</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - genetics</topic><topic>Oxygen - metabolism</topic><topic>PC12 cell</topic><topic>PC12 Cells</topic><topic>Pharmacology. Drug treatments</topic><topic>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Rats</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Stilbenes - pharmacology</topic><topic>Trans resveratrol</topic><topic>Transcription, Genetic - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Agrawal, Megha</creatorcontrib><creatorcontrib>Kumar, Vivek</creatorcontrib><creatorcontrib>Kashyap, Mahendra P.</creatorcontrib><creatorcontrib>Khanna, Vinay K.</creatorcontrib><creatorcontrib>Randhawa, Gursharn S.</creatorcontrib><creatorcontrib>Pant, Aditya B.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Agrawal, Megha</au><au>Kumar, Vivek</au><au>Kashyap, Mahendra P.</au><au>Khanna, Vinay K.</au><au>Randhawa, Gursharn S.</au><au>Pant, Aditya B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ischemic insult induced apoptotic changes in PC12 cells: Protection by trans resveratrol</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2011-09-01</date><risdate>2011</risdate><volume>666</volume><issue>1</issue><spage>5</spage><epage>11</epage><pages>5-11</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>In this study, we determined the protective potential of
trans resveratrol against oxygen–glucose deprivation (OGD) induced reactive oxygen species mediated apoptotic damages in PC12 cells. In vitro model of ischemic cerebral stroke was created by keeping cells in an OGD condition for 6
h followed by 24
h reoxygenation. Cells received biologically safe doses (5, 10, and 25
μM) of
trans resveratrol in the following schedules for 24
h prior to OGD; during 6
h of OGD; for 24
h post OGD and whole treatment group which starts from 24
h before OGD and lasted to 24
h post OGD. Anti-ischemic potential of
trans resveratrol was assessed by measuring the regulation of lipid peroxidation, reactive oxygen species production, glutathione content, and expression (mRNA and protein) of apoptotic markers such as Bax, Bcl
2 and Caspase-3. Hypoxia inducible factor-1α (HIF-1α) was also assessed to correlate the changes with ischemic injuries. Significant (P
<
0.05) restoration in lipid peroxidation, reactive oxygen species, and glutathione content were observed following the treatment of
trans resveratrol in cells receiving OGD and re-oxygenation. Changes induced by
trans resveratrol could be correlated well with alterations in the expression of Bax, Bcl
2, Caspase-3 and HIF-1α. These results indicate that
trans resveratrol administration attenuates free radical formation and mitochondria mediated apoptosis perhaps by regulating the expressions of Bax, Bcl
2, and Caspase-3 in PC12 cells receiving OGD and re-oxygenation insult.
[Display omitted]</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>21620820</pmid><doi>10.1016/j.ejphar.2011.05.015</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | European journal of pharmacology, 2011-09, Vol.666 (1), p.5-11 |
| issn | 0014-2999 1879-0712 |
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| subjects | Animals Apoptosis Apoptosis - drug effects Apoptosis - genetics bcl-2-Associated X Protein - biosynthesis bcl-2-Associated X Protein - genetics Biological and medical sciences Brain Ischemia - genetics Brain Ischemia - metabolism Brain Ischemia - pathology Brain Ischemia - prevention & control Caspase 3 - biosynthesis Caspase 3 - genetics Glucose - metabolism Glutathione - metabolism Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis Hypoxia-Inducible Factor 1, alpha Subunit - genetics Lipid Peroxidation - drug effects Medical sciences Neurons - drug effects Neurons - metabolism Neurons - pathology Neuroprotection Neuroprotective Agents - pharmacology OGD Oxidative Stress - drug effects Oxidative Stress - genetics Oxygen - metabolism PC12 cell PC12 Cells Pharmacology. Drug treatments Proto-Oncogene Proteins c-bcl-2 - biosynthesis Proto-Oncogene Proteins c-bcl-2 - genetics Rats Reactive Oxygen Species - metabolism Stilbenes - pharmacology Trans resveratrol Transcription, Genetic - drug effects |
| title | Ischemic insult induced apoptotic changes in PC12 cells: Protection by trans resveratrol |
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