Curcumin Protects Against Regional Myocardial Ischemia/Reperfusion Injury Through Activation of RISK/GSK-3β and Inhibition of p38 MAPK and JNK
Background: Curcumin, the active ingredient of turmeric (Curcuma longa), is known to have anti-inflammatory and antioxidative properties. The present study was aimed to determine the effect of curcumin in regional myocardial ischemia/reperfusion (I/R) injury and its underlying mechanisms involving t...
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| Veröffentlicht in: | Journal of cardiovascular pharmacology and therapeutics 2012-12, Vol.17 (4), p.387-394 |
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| creator | Jeong, Cheol-Won Yoo, Kyung Yeon Lee, Seong Heon Jeong, Hye Jin Lee, Cha Sup Kim, Seok Jai |
| description | Background:
Curcumin, the active ingredient of turmeric (Curcuma longa), is known to have anti-inflammatory and antioxidative properties. The present study was aimed to determine the effect of curcumin in regional myocardial ischemia/reperfusion (I/R) injury and its underlying mechanisms involving the role of prosurvival kinases and apoptotic kinases.
Methods:
Sprague-Dawley rats (n = 109) subjected to a 30-minute left anterior descending coronary artery (LAD) occlusion followed by reperfusion were assigned to receive saline (control), curcumin (100 mg/kg), wortmannin (inhibitor of phosphatidylinositol-3-OH kinase [PI3K]-Akt), wortmannin + curcumin, U0126 (inhibitor of extracellular signal-regulated kinase [ERK1/2]), U0126 + curcumin, SB216763 (inhibitor of glycogen synthase kinase [GSK-3β]), and SB216763 + curcumin 20 minutes before LAD occlusion. Infarct size was measured after 2 hours of reperfusion by triphenyl tetrazolium chloride staining. The phosphorylation of Akt, ERK1/2, GSK-3β, p38, and c-Jun N-terminal kinases (JNK) was determined by immunoblotting after 10 minutes of reperfusion.
Results:
Curcumin significantly reduced the infarct size compared with the control (33.1% ± 6.2% vs 50.1% ± 3.9%; P < .05). Wortmannin or U0126 alone did not affect the infarct size but abolished the curcumin-induced cardioprotective effect. Curcumin significantly enhanced the phosphorylation of Akt, ERK1/2, and GSK-3β, while it reduced that of p38 and JNK. Wortmannin or U0126 abolished enhanced phosphorylation of GSK-3β induced by curcumin. SB216763 alone or combined with curcumin reduced the infarct size and enhanced phosphorylation of GSK-3β compared with the control.
Conclusions:
Preconditioning by curcumin effectively protects against regional myocardial I/R injury through the activation of prosurvival kinases involving PI3K-Akt, ERK1/2, and GSK-3β, and attenuation of p38 and JNK. |
| doi_str_mv | 10.1177/1074248412438102 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_AFRWT</sourceid><recordid>TN_cdi_proquest_miscellaneous_1143835346</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_1074248412438102</sage_id><sourcerecordid>1143835346</sourcerecordid><originalsourceid>FETCH-LOGICAL-c337t-6ccc20970d036f7f77bc720b09687119d9a3bd71a23e6327034e22c5d52dc23b3</originalsourceid><addsrcrecordid>eNp1kc9OAjEQxhujEUTvnkyPXlb6Z9nuHglRREAJ4HnT7XahhN1iuzXhKXwXH8Rnsgh4MPE0k_l-8yXzDQDXGN1hzFgbIxaSMA4xCWmMETkBTZyEKAgRDU997-VgpzfAhbUrhPy4k5yDBiE0iSiJm-Cj54xwpargxOhaitrC7oKrytZwKhdKV3wNx1stuMmVbwdWLGWpeHsqN9IUznoCDqqVM1s4XxrtFkvYFbV65_VO0QWcDmbDdn82DOjXJ-RV7umlytRR3tAYjruT4Y_09Dy8BGcFX1t5dagt8PpwP-89BqOX_qDXHQWCUlYHkRCCoIShHNGoYAVjmWAEZSiJYoZxkiecZjnDnFDpD2X-cEmI6OQdkgtCM9oCt3vfjdFvTto6LZUVcr3mldTOphj7RGmHhpFH0R4VRltrZJFujCq52aYYpbs3pH_f4FduDu4uK2X-u3DM3QPBHrB8IdOVdsYHbf83_AZnM46y</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1143835346</pqid></control><display><type>article</type><title>Curcumin Protects Against Regional Myocardial Ischemia/Reperfusion Injury Through Activation of RISK/GSK-3β and Inhibition of p38 MAPK and JNK</title><source>Sage Journals GOLD Open Access 2024</source><creator>Jeong, Cheol-Won ; Yoo, Kyung Yeon ; Lee, Seong Heon ; Jeong, Hye Jin ; Lee, Cha Sup ; Kim, Seok Jai</creator><creatorcontrib>Jeong, Cheol-Won ; Yoo, Kyung Yeon ; Lee, Seong Heon ; Jeong, Hye Jin ; Lee, Cha Sup ; Kim, Seok Jai</creatorcontrib><description>Background:
Curcumin, the active ingredient of turmeric (Curcuma longa), is known to have anti-inflammatory and antioxidative properties. The present study was aimed to determine the effect of curcumin in regional myocardial ischemia/reperfusion (I/R) injury and its underlying mechanisms involving the role of prosurvival kinases and apoptotic kinases.
Methods:
Sprague-Dawley rats (n = 109) subjected to a 30-minute left anterior descending coronary artery (LAD) occlusion followed by reperfusion were assigned to receive saline (control), curcumin (100 mg/kg), wortmannin (inhibitor of phosphatidylinositol-3-OH kinase [PI3K]-Akt), wortmannin + curcumin, U0126 (inhibitor of extracellular signal-regulated kinase [ERK1/2]), U0126 + curcumin, SB216763 (inhibitor of glycogen synthase kinase [GSK-3β]), and SB216763 + curcumin 20 minutes before LAD occlusion. Infarct size was measured after 2 hours of reperfusion by triphenyl tetrazolium chloride staining. The phosphorylation of Akt, ERK1/2, GSK-3β, p38, and c-Jun N-terminal kinases (JNK) was determined by immunoblotting after 10 minutes of reperfusion.
Results:
Curcumin significantly reduced the infarct size compared with the control (33.1% ± 6.2% vs 50.1% ± 3.9%; P < .05). Wortmannin or U0126 alone did not affect the infarct size but abolished the curcumin-induced cardioprotective effect. Curcumin significantly enhanced the phosphorylation of Akt, ERK1/2, and GSK-3β, while it reduced that of p38 and JNK. Wortmannin or U0126 abolished enhanced phosphorylation of GSK-3β induced by curcumin. SB216763 alone or combined with curcumin reduced the infarct size and enhanced phosphorylation of GSK-3β compared with the control.
Conclusions:
Preconditioning by curcumin effectively protects against regional myocardial I/R injury through the activation of prosurvival kinases involving PI3K-Akt, ERK1/2, and GSK-3β, and attenuation of p38 and JNK.</description><identifier>ISSN: 1074-2484</identifier><identifier>EISSN: 1940-4034</identifier><identifier>DOI: 10.1177/1074248412438102</identifier><identifier>PMID: 22396328</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject><![CDATA[Animals ; Anti-Inflammatory Agents, Non-Steroidal - antagonists & inhibitors ; Anti-Inflammatory Agents, Non-Steroidal - therapeutic use ; Antioxidants - chemistry ; Antioxidants - therapeutic use ; Cardiotonic Agents - antagonists & inhibitors ; Cardiotonic Agents - therapeutic use ; Curcumin - chemistry ; Curcumin - therapeutic use ; Drug Therapy, Combination ; Enzyme Inhibitors - adverse effects ; Enzyme Inhibitors - therapeutic use ; Glycogen Synthase Kinase 3 - antagonists & inhibitors ; Glycogen Synthase Kinase 3 - chemistry ; Glycogen Synthase Kinase 3 - metabolism ; Glycogen Synthase Kinase 3 beta ; Heart Ventricles - drug effects ; Heart Ventricles - enzymology ; Heart Ventricles - pathology ; Indoles - therapeutic use ; Male ; Maleimides - therapeutic use ; MAP Kinase Signaling System - drug effects ; Myocardial Infarction - etiology ; Myocardial Infarction - pathology ; Myocardial Infarction - prevention & control ; Myocardial Reperfusion Injury - enzymology ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - prevention & control ; Phosphatidylinositol 3-Kinase - antagonists & inhibitors ; Phosphatidylinositol 3-Kinase - metabolism ; Phosphorylation - drug effects ; Protein Processing, Post-Translational - drug effects ; Proto-Oncogene Proteins c-akt - antagonists & inhibitors ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Sprague-Dawley]]></subject><ispartof>Journal of cardiovascular pharmacology and therapeutics, 2012-12, Vol.17 (4), p.387-394</ispartof><rights>The Author(s) 2012</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c337t-6ccc20970d036f7f77bc720b09687119d9a3bd71a23e6327034e22c5d52dc23b3</citedby><cites>FETCH-LOGICAL-c337t-6ccc20970d036f7f77bc720b09687119d9a3bd71a23e6327034e22c5d52dc23b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/1074248412438102$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/1074248412438102$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,776,780,21945,27830,27901,27902,44921,45309</link.rule.ids><linktorsrc>$$Uhttps://journals.sagepub.com/doi/full/10.1177/1074248412438102?utm_source=summon&utm_medium=discovery-provider$$EView_record_in_SAGE_Publications$$FView_record_in_$$GSAGE_Publications</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22396328$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jeong, Cheol-Won</creatorcontrib><creatorcontrib>Yoo, Kyung Yeon</creatorcontrib><creatorcontrib>Lee, Seong Heon</creatorcontrib><creatorcontrib>Jeong, Hye Jin</creatorcontrib><creatorcontrib>Lee, Cha Sup</creatorcontrib><creatorcontrib>Kim, Seok Jai</creatorcontrib><title>Curcumin Protects Against Regional Myocardial Ischemia/Reperfusion Injury Through Activation of RISK/GSK-3β and Inhibition of p38 MAPK and JNK</title><title>Journal of cardiovascular pharmacology and therapeutics</title><addtitle>J Cardiovasc Pharmacol Ther</addtitle><description>Background:
Curcumin, the active ingredient of turmeric (Curcuma longa), is known to have anti-inflammatory and antioxidative properties. The present study was aimed to determine the effect of curcumin in regional myocardial ischemia/reperfusion (I/R) injury and its underlying mechanisms involving the role of prosurvival kinases and apoptotic kinases.
Methods:
Sprague-Dawley rats (n = 109) subjected to a 30-minute left anterior descending coronary artery (LAD) occlusion followed by reperfusion were assigned to receive saline (control), curcumin (100 mg/kg), wortmannin (inhibitor of phosphatidylinositol-3-OH kinase [PI3K]-Akt), wortmannin + curcumin, U0126 (inhibitor of extracellular signal-regulated kinase [ERK1/2]), U0126 + curcumin, SB216763 (inhibitor of glycogen synthase kinase [GSK-3β]), and SB216763 + curcumin 20 minutes before LAD occlusion. Infarct size was measured after 2 hours of reperfusion by triphenyl tetrazolium chloride staining. The phosphorylation of Akt, ERK1/2, GSK-3β, p38, and c-Jun N-terminal kinases (JNK) was determined by immunoblotting after 10 minutes of reperfusion.
Results:
Curcumin significantly reduced the infarct size compared with the control (33.1% ± 6.2% vs 50.1% ± 3.9%; P < .05). Wortmannin or U0126 alone did not affect the infarct size but abolished the curcumin-induced cardioprotective effect. Curcumin significantly enhanced the phosphorylation of Akt, ERK1/2, and GSK-3β, while it reduced that of p38 and JNK. Wortmannin or U0126 abolished enhanced phosphorylation of GSK-3β induced by curcumin. SB216763 alone or combined with curcumin reduced the infarct size and enhanced phosphorylation of GSK-3β compared with the control.
Conclusions:
Preconditioning by curcumin effectively protects against regional myocardial I/R injury through the activation of prosurvival kinases involving PI3K-Akt, ERK1/2, and GSK-3β, and attenuation of p38 and JNK.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - antagonists & inhibitors</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - therapeutic use</subject><subject>Antioxidants - chemistry</subject><subject>Antioxidants - therapeutic use</subject><subject>Cardiotonic Agents - antagonists & inhibitors</subject><subject>Cardiotonic Agents - therapeutic use</subject><subject>Curcumin - chemistry</subject><subject>Curcumin - therapeutic use</subject><subject>Drug Therapy, Combination</subject><subject>Enzyme Inhibitors - adverse effects</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Glycogen Synthase Kinase 3 - antagonists & inhibitors</subject><subject>Glycogen Synthase Kinase 3 - chemistry</subject><subject>Glycogen Synthase Kinase 3 - metabolism</subject><subject>Glycogen Synthase Kinase 3 beta</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - enzymology</subject><subject>Heart Ventricles - pathology</subject><subject>Indoles - therapeutic use</subject><subject>Male</subject><subject>Maleimides - therapeutic use</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Myocardial Infarction - etiology</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - prevention & control</subject><subject>Myocardial Reperfusion Injury - enzymology</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Phosphatidylinositol 3-Kinase - antagonists & inhibitors</subject><subject>Phosphatidylinositol 3-Kinase - metabolism</subject><subject>Phosphorylation - drug effects</subject><subject>Protein Processing, Post-Translational - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - antagonists & inhibitors</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>1074-2484</issn><issn>1940-4034</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9OAjEQxhujEUTvnkyPXlb6Z9nuHglRREAJ4HnT7XahhN1iuzXhKXwXH8Rnsgh4MPE0k_l-8yXzDQDXGN1hzFgbIxaSMA4xCWmMETkBTZyEKAgRDU997-VgpzfAhbUrhPy4k5yDBiE0iSiJm-Cj54xwpargxOhaitrC7oKrytZwKhdKV3wNx1stuMmVbwdWLGWpeHsqN9IUznoCDqqVM1s4XxrtFkvYFbV65_VO0QWcDmbDdn82DOjXJ-RV7umlytRR3tAYjruT4Y_09Dy8BGcFX1t5dagt8PpwP-89BqOX_qDXHQWCUlYHkRCCoIShHNGoYAVjmWAEZSiJYoZxkiecZjnDnFDpD2X-cEmI6OQdkgtCM9oCt3vfjdFvTto6LZUVcr3mldTOphj7RGmHhpFH0R4VRltrZJFujCq52aYYpbs3pH_f4FduDu4uK2X-u3DM3QPBHrB8IdOVdsYHbf83_AZnM46y</recordid><startdate>201212</startdate><enddate>201212</enddate><creator>Jeong, Cheol-Won</creator><creator>Yoo, Kyung Yeon</creator><creator>Lee, Seong Heon</creator><creator>Jeong, Hye Jin</creator><creator>Lee, Cha Sup</creator><creator>Kim, Seok Jai</creator><general>SAGE Publications</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>7X8</scope></search><sort><creationdate>201212</creationdate><title>Curcumin Protects Against Regional Myocardial Ischemia/Reperfusion Injury Through Activation of RISK/GSK-3β and Inhibition of p38 MAPK and JNK</title><author>Jeong, Cheol-Won ; Yoo, Kyung Yeon ; Lee, Seong Heon ; Jeong, Hye Jin ; Lee, Cha Sup ; Kim, Seok Jai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c337t-6ccc20970d036f7f77bc720b09687119d9a3bd71a23e6327034e22c5d52dc23b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - antagonists & inhibitors</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - therapeutic use</topic><topic>Antioxidants - chemistry</topic><topic>Antioxidants - therapeutic use</topic><topic>Cardiotonic Agents - antagonists & inhibitors</topic><topic>Cardiotonic Agents - therapeutic use</topic><topic>Curcumin - chemistry</topic><topic>Curcumin - therapeutic use</topic><topic>Drug Therapy, Combination</topic><topic>Enzyme Inhibitors - adverse effects</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Glycogen Synthase Kinase 3 - antagonists & inhibitors</topic><topic>Glycogen Synthase Kinase 3 - chemistry</topic><topic>Glycogen Synthase Kinase 3 - metabolism</topic><topic>Glycogen Synthase Kinase 3 beta</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - enzymology</topic><topic>Heart Ventricles - pathology</topic><topic>Indoles - therapeutic use</topic><topic>Male</topic><topic>Maleimides - therapeutic use</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Myocardial Infarction - etiology</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - prevention & control</topic><topic>Myocardial Reperfusion Injury - enzymology</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Phosphatidylinositol 3-Kinase - antagonists & inhibitors</topic><topic>Phosphatidylinositol 3-Kinase - metabolism</topic><topic>Phosphorylation - drug effects</topic><topic>Protein Processing, Post-Translational - drug effects</topic><topic>Proto-Oncogene Proteins c-akt - antagonists & inhibitors</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><toplevel>online_resources</toplevel><creatorcontrib>Jeong, Cheol-Won</creatorcontrib><creatorcontrib>Yoo, Kyung Yeon</creatorcontrib><creatorcontrib>Lee, Seong Heon</creatorcontrib><creatorcontrib>Jeong, Hye Jin</creatorcontrib><creatorcontrib>Lee, Cha Sup</creatorcontrib><creatorcontrib>Kim, Seok Jai</creatorcontrib><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>Journal of cardiovascular pharmacology and therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Jeong, Cheol-Won</au><au>Yoo, Kyung Yeon</au><au>Lee, Seong Heon</au><au>Jeong, Hye Jin</au><au>Lee, Cha Sup</au><au>Kim, Seok Jai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Curcumin Protects Against Regional Myocardial Ischemia/Reperfusion Injury Through Activation of RISK/GSK-3β and Inhibition of p38 MAPK and JNK</atitle><jtitle>Journal of cardiovascular pharmacology and therapeutics</jtitle><addtitle>J Cardiovasc Pharmacol Ther</addtitle><date>2012-12</date><risdate>2012</risdate><volume>17</volume><issue>4</issue><spage>387</spage><epage>394</epage><pages>387-394</pages><issn>1074-2484</issn><eissn>1940-4034</eissn><abstract>Background:
Curcumin, the active ingredient of turmeric (Curcuma longa), is known to have anti-inflammatory and antioxidative properties. The present study was aimed to determine the effect of curcumin in regional myocardial ischemia/reperfusion (I/R) injury and its underlying mechanisms involving the role of prosurvival kinases and apoptotic kinases.
Methods:
Sprague-Dawley rats (n = 109) subjected to a 30-minute left anterior descending coronary artery (LAD) occlusion followed by reperfusion were assigned to receive saline (control), curcumin (100 mg/kg), wortmannin (inhibitor of phosphatidylinositol-3-OH kinase [PI3K]-Akt), wortmannin + curcumin, U0126 (inhibitor of extracellular signal-regulated kinase [ERK1/2]), U0126 + curcumin, SB216763 (inhibitor of glycogen synthase kinase [GSK-3β]), and SB216763 + curcumin 20 minutes before LAD occlusion. Infarct size was measured after 2 hours of reperfusion by triphenyl tetrazolium chloride staining. The phosphorylation of Akt, ERK1/2, GSK-3β, p38, and c-Jun N-terminal kinases (JNK) was determined by immunoblotting after 10 minutes of reperfusion.
Results:
Curcumin significantly reduced the infarct size compared with the control (33.1% ± 6.2% vs 50.1% ± 3.9%; P < .05). Wortmannin or U0126 alone did not affect the infarct size but abolished the curcumin-induced cardioprotective effect. Curcumin significantly enhanced the phosphorylation of Akt, ERK1/2, and GSK-3β, while it reduced that of p38 and JNK. Wortmannin or U0126 abolished enhanced phosphorylation of GSK-3β induced by curcumin. SB216763 alone or combined with curcumin reduced the infarct size and enhanced phosphorylation of GSK-3β compared with the control.
Conclusions:
Preconditioning by curcumin effectively protects against regional myocardial I/R injury through the activation of prosurvival kinases involving PI3K-Akt, ERK1/2, and GSK-3β, and attenuation of p38 and JNK.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>22396328</pmid><doi>10.1177/1074248412438102</doi><tpages>8</tpages></addata></record> |
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| ispartof | Journal of cardiovascular pharmacology and therapeutics, 2012-12, Vol.17 (4), p.387-394 |
| issn | 1074-2484 1940-4034 |
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| source | Sage Journals GOLD Open Access 2024 |
| subjects | Animals Anti-Inflammatory Agents, Non-Steroidal - antagonists & inhibitors Anti-Inflammatory Agents, Non-Steroidal - therapeutic use Antioxidants - chemistry Antioxidants - therapeutic use Cardiotonic Agents - antagonists & inhibitors Cardiotonic Agents - therapeutic use Curcumin - chemistry Curcumin - therapeutic use Drug Therapy, Combination Enzyme Inhibitors - adverse effects Enzyme Inhibitors - therapeutic use Glycogen Synthase Kinase 3 - antagonists & inhibitors Glycogen Synthase Kinase 3 - chemistry Glycogen Synthase Kinase 3 - metabolism Glycogen Synthase Kinase 3 beta Heart Ventricles - drug effects Heart Ventricles - enzymology Heart Ventricles - pathology Indoles - therapeutic use Male Maleimides - therapeutic use MAP Kinase Signaling System - drug effects Myocardial Infarction - etiology Myocardial Infarction - pathology Myocardial Infarction - prevention & control Myocardial Reperfusion Injury - enzymology Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - prevention & control Phosphatidylinositol 3-Kinase - antagonists & inhibitors Phosphatidylinositol 3-Kinase - metabolism Phosphorylation - drug effects Protein Processing, Post-Translational - drug effects Proto-Oncogene Proteins c-akt - antagonists & inhibitors Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Sprague-Dawley |
| title | Curcumin Protects Against Regional Myocardial Ischemia/Reperfusion Injury Through Activation of RISK/GSK-3β and Inhibition of p38 MAPK and JNK |
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