A Synthetic Epoxydocosapentaenoic Acid Analogue Ameliorates Cardiac Ischemia/Reperfusion Injury: The Involvement of the Sirtuin 3-NLRP3 Pathway
While survival rates have markedly improved following cardiac ischemia-reperfusion (IR) injury, the resulting heart damage remains an important issue. Preserving mitochondrial quality and limiting NLRP3 inflammasome activation is an approach to limit IR injury, in which the mitochondrial deacetylase...
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| Veröffentlicht in: | International journal of molecular sciences 2020-07, Vol.21 (15), p.5261 |
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| creator | Darwesh, Ahmed M Bassiouni, Wesam Adebesin, Adeniyi Michael Mohammad, Abdul Sattar Falck, John R Seubert, John M |
| description | While survival rates have markedly improved following cardiac ischemia-reperfusion (IR) injury, the resulting heart damage remains an important issue. Preserving mitochondrial quality and limiting NLRP3 inflammasome activation is an approach to limit IR injury, in which the mitochondrial deacetylase sirtuin 3 (SIRT3) has a role. Recent data demonstrate cytochrome P450 (CYP450)-derived epoxy metabolites, epoxydocosapentaenoic acids (EDPs), of docosahexaenoic acid (DHA), attenuate cardiac IR injury. EDPs undergo rapid removal and inactivation by enzymatic and non-enzymatic processes. The current study hypothesizes that the cardioprotective effects of the synthetic EDP surrogates AS-27, SA-26 and AA-4 against IR injury involve activation of SIRT3. Isolated hearts from wild type (WT) mice were perfused in the Langendorff mode with vehicle, AS-27, SA-26 or AA-4. Improved postischemic functional recovery, maintained cardiac ATP levels, reduced oxidative stress and attenuation of NLRP3 activation were observed in hearts perfused with the analogue SA-26. Assessment of cardiac mitochondria demonstrated SA-26 preserved SIRT3 activity and reduced acetylation of manganese superoxide dismutase (MnSOD) suggesting enhanced antioxidant capacity. Together, these data demonstrate that the cardioprotective effects of the EDP analogue SA-26 against IR injury involve preservation of mitochondrial SIRT3 activity, which attenuates a detrimental innate NLRP3 inflammasome response. |
| doi_str_mv | 10.3390/ijms21155261 |
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Preserving mitochondrial quality and limiting NLRP3 inflammasome activation is an approach to limit IR injury, in which the mitochondrial deacetylase sirtuin 3 (SIRT3) has a role. Recent data demonstrate cytochrome P450 (CYP450)-derived epoxy metabolites, epoxydocosapentaenoic acids (EDPs), of docosahexaenoic acid (DHA), attenuate cardiac IR injury. EDPs undergo rapid removal and inactivation by enzymatic and non-enzymatic processes. The current study hypothesizes that the cardioprotective effects of the synthetic EDP surrogates AS-27, SA-26 and AA-4 against IR injury involve activation of SIRT3. Isolated hearts from wild type (WT) mice were perfused in the Langendorff mode with vehicle, AS-27, SA-26 or AA-4. Improved postischemic functional recovery, maintained cardiac ATP levels, reduced oxidative stress and attenuation of NLRP3 activation were observed in hearts perfused with the analogue SA-26. Assessment of cardiac mitochondria demonstrated SA-26 preserved SIRT3 activity and reduced acetylation of manganese superoxide dismutase (MnSOD) suggesting enhanced antioxidant capacity. Together, these data demonstrate that the cardioprotective effects of the EDP analogue SA-26 against IR injury involve preservation of mitochondrial SIRT3 activity, which attenuates a detrimental innate NLRP3 inflammasome response.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms21155261</identifier><identifier>PMID: 32722183</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acetylation ; Activation ; Animals ; Antioxidants ; Attenuation ; Cytochrome P450 ; Cytochromes P450 ; Docosahexaenoic acid ; Docosahexaenoic Acids - analogs & derivatives ; Docosahexaenoic Acids - chemical synthesis ; Docosahexaenoic Acids - chemistry ; Docosahexaenoic Acids - pharmacology ; Enzymes ; Female ; Heart ; Homeostasis ; Inflammasomes ; Injury prevention ; Ischemia ; Male ; Manganese ; Metabolites ; Mice ; Mitochondria ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocardium - metabolism ; Myocardium - pathology ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Oxidative stress ; Oxidative Stress - drug effects ; Preservation ; Proteins ; Recovery of function ; Reperfusion ; Sirtuin 3 - metabolism ; Superoxide dismutase</subject><ispartof>International journal of molecular sciences, 2020-07, Vol.21 (15), p.5261</ispartof><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). 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Preserving mitochondrial quality and limiting NLRP3 inflammasome activation is an approach to limit IR injury, in which the mitochondrial deacetylase sirtuin 3 (SIRT3) has a role. Recent data demonstrate cytochrome P450 (CYP450)-derived epoxy metabolites, epoxydocosapentaenoic acids (EDPs), of docosahexaenoic acid (DHA), attenuate cardiac IR injury. EDPs undergo rapid removal and inactivation by enzymatic and non-enzymatic processes. The current study hypothesizes that the cardioprotective effects of the synthetic EDP surrogates AS-27, SA-26 and AA-4 against IR injury involve activation of SIRT3. Isolated hearts from wild type (WT) mice were perfused in the Langendorff mode with vehicle, AS-27, SA-26 or AA-4. Improved postischemic functional recovery, maintained cardiac ATP levels, reduced oxidative stress and attenuation of NLRP3 activation were observed in hearts perfused with the analogue SA-26. Assessment of cardiac mitochondria demonstrated SA-26 preserved SIRT3 activity and reduced acetylation of manganese superoxide dismutase (MnSOD) suggesting enhanced antioxidant capacity. Together, these data demonstrate that the cardioprotective effects of the EDP analogue SA-26 against IR injury involve preservation of mitochondrial SIRT3 activity, which attenuates a detrimental innate NLRP3 inflammasome response.</description><subject>Acetylation</subject><subject>Activation</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Attenuation</subject><subject>Cytochrome P450</subject><subject>Cytochromes P450</subject><subject>Docosahexaenoic acid</subject><subject>Docosahexaenoic Acids - analogs & derivatives</subject><subject>Docosahexaenoic Acids - chemical synthesis</subject><subject>Docosahexaenoic Acids - chemistry</subject><subject>Docosahexaenoic Acids - pharmacology</subject><subject>Enzymes</subject><subject>Female</subject><subject>Heart</subject><subject>Homeostasis</subject><subject>Inflammasomes</subject><subject>Injury prevention</subject><subject>Ischemia</subject><subject>Male</subject><subject>Manganese</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Mitochondria</subject><subject>Myocardial Reperfusion Injury - 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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>Darwesh, Ahmed M</au><au>Bassiouni, Wesam</au><au>Adebesin, Adeniyi Michael</au><au>Mohammad, Abdul Sattar</au><au>Falck, John R</au><au>Seubert, John M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Synthetic Epoxydocosapentaenoic Acid Analogue Ameliorates Cardiac Ischemia/Reperfusion Injury: The Involvement of the Sirtuin 3-NLRP3 Pathway</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2020-07-24</date><risdate>2020</risdate><volume>21</volume><issue>15</issue><spage>5261</spage><pages>5261-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>While survival rates have markedly improved following cardiac ischemia-reperfusion (IR) injury, the resulting heart damage remains an important issue. Preserving mitochondrial quality and limiting NLRP3 inflammasome activation is an approach to limit IR injury, in which the mitochondrial deacetylase sirtuin 3 (SIRT3) has a role. Recent data demonstrate cytochrome P450 (CYP450)-derived epoxy metabolites, epoxydocosapentaenoic acids (EDPs), of docosahexaenoic acid (DHA), attenuate cardiac IR injury. EDPs undergo rapid removal and inactivation by enzymatic and non-enzymatic processes. The current study hypothesizes that the cardioprotective effects of the synthetic EDP surrogates AS-27, SA-26 and AA-4 against IR injury involve activation of SIRT3. Isolated hearts from wild type (WT) mice were perfused in the Langendorff mode with vehicle, AS-27, SA-26 or AA-4. Improved postischemic functional recovery, maintained cardiac ATP levels, reduced oxidative stress and attenuation of NLRP3 activation were observed in hearts perfused with the analogue SA-26. Assessment of cardiac mitochondria demonstrated SA-26 preserved SIRT3 activity and reduced acetylation of manganese superoxide dismutase (MnSOD) suggesting enhanced antioxidant capacity. Together, these data demonstrate that the cardioprotective effects of the EDP analogue SA-26 against IR injury involve preservation of mitochondrial SIRT3 activity, which attenuates a detrimental innate NLRP3 inflammasome response.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>32722183</pmid><doi>10.3390/ijms21155261</doi><orcidid>https://orcid.org/0000-0002-9219-7845</orcidid><orcidid>https://orcid.org/0000-0002-7424-2681</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acetylation Activation Animals Antioxidants Attenuation Cytochrome P450 Cytochromes P450 Docosahexaenoic acid Docosahexaenoic Acids - analogs & derivatives Docosahexaenoic Acids - chemical synthesis Docosahexaenoic Acids - chemistry Docosahexaenoic Acids - pharmacology Enzymes Female Heart Homeostasis Inflammasomes Injury prevention Ischemia Male Manganese Metabolites Mice Mitochondria Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardium - metabolism Myocardium - pathology NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Oxidative stress Oxidative Stress - drug effects Preservation Proteins Recovery of function Reperfusion Sirtuin 3 - metabolism Superoxide dismutase |
| title | A Synthetic Epoxydocosapentaenoic Acid Analogue Ameliorates Cardiac Ischemia/Reperfusion Injury: The Involvement of the Sirtuin 3-NLRP3 Pathway |
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