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Endogenous generation and protective effects of nitro-fatty acids in a murine model of focal cardiac ischaemia and reperfusion

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Endogenous generation and protective effects of nitro-fatty acids in a murine model of focal cardiac ischaemia and reperfusion. / Rudolph, Volker; Rudolph, Tanja K; Schopfer, Francisco J; Bonacci, Gustavo; Woodcock, Steven R; Cole, Marsha P; Baker, Paul R S; Ramani, Ravi; Freeman, Bruce A.

In: CARDIOVASC RES, Vol. 85, No. 1, 01.01.2010, p. 155-166.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Rudolph, V, Rudolph, TK, Schopfer, FJ, Bonacci, G, Woodcock, SR, Cole, MP, Baker, PRS, Ramani, R & Freeman, BA 2010, 'Endogenous generation and protective effects of nitro-fatty acids in a murine model of focal cardiac ischaemia and reperfusion', CARDIOVASC RES, vol. 85, no. 1, pp. 155-166. https://doi.org/10.1093/cvr/cvp275

APA

Rudolph, V., Rudolph, T. K., Schopfer, F. J., Bonacci, G., Woodcock, S. R., Cole, M. P., Baker, P. R. S., Ramani, R., & Freeman, B. A. (2010). Endogenous generation and protective effects of nitro-fatty acids in a murine model of focal cardiac ischaemia and reperfusion. CARDIOVASC RES, 85(1), 155-166. https://doi.org/10.1093/cvr/cvp275

Vancouver

Rudolph V, Rudolph TK, Schopfer FJ, Bonacci G, Woodcock SR, Cole MP et al. Endogenous generation and protective effects of nitro-fatty acids in a murine model of focal cardiac ischaemia and reperfusion. CARDIOVASC RES. 2010 Jan 1;85(1):155-166. https://doi.org/10.1093/cvr/cvp275

Bibtex

@article{7f0554c63bfd4a82a37e7d6288c03923,
title = "Endogenous generation and protective effects of nitro-fatty acids in a murine model of focal cardiac ischaemia and reperfusion",
abstract = "AIMS: Nitrated fatty acids (NO(2)-FA) have been identified as endogenous anti-inflammatory signalling mediators generated by oxidative inflammatory reactions. Herein the in vivo generation of nitro-oleic acid (OA-NO(2)) and nitro-linoleic acid (LNO(2)) was measured in a murine model of myocardial ischaemia and reperfusion (I/R) and the effect of exogenous administration of OA-NO(2) on I/R injury was evaluated.METHODS AND RESULTS: In C57/BL6 mice subjected to 30 min of coronary artery ligation, endogenous OA-NO(2) and LNO(2) formation was observed after 30 min of reperfusion, whereas no NO(2)-FA were detected in sham-operated mice and mice with myocardial infarction without reperfusion. Exogenous administration of 20 nmol/g body weight OA-NO(2) during the ischaemic episode induced profound protection against I/R injury with a 46% reduction in infarct size (normalized to area at risk) and a marked preservation of left ventricular function as assessed by transthoracic echocardiography, compared with vehicle-treated mice. Administration of OA-NO(2) inhibited activation of the p65 subunit of nuclear factor kappaB (NFkappaB) in I/R tissue. Experiments using the NFkappaB inhibitor pyrrolidinedithiocarbamate also support that protection lent by OA-NO(2) was in part mediated by inhibition of NFkappaB. OA-NO(2) inhibition of NFkappaB activation was accompanied by suppression of downstream intercellular adhesion molecule 1 and monocyte chemotactic protein 1 expression, neutrophil infiltration, and myocyte apoptosis.CONCLUSION: This study reveals the de novo generation of fatty acid nitration products in vivo and reveals the anti-inflammatory and potential therapeutic actions of OA-NO(2) in myocardial I/R injury.",
keywords = "Alkylation, Animals, Apoptosis, Disease Models, Animal, Echocardiography, Fatty Acids/metabolism, Inflammation/etiology, Male, Mice, Mice, Inbred C57BL, Myocardial Ischemia/metabolism, Myocardial Reperfusion Injury/prevention & control, Neutrophil Infiltration, Nitric Oxide/metabolism, Proline/analogs & derivatives, Thiocarbamates/pharmacology, Transcription Factor RelA/metabolism",
author = "Volker Rudolph and Rudolph, {Tanja K} and Schopfer, {Francisco J} and Gustavo Bonacci and Woodcock, {Steven R} and Cole, {Marsha P} and Baker, {Paul R S} and Ravi Ramani and Freeman, {Bruce A}",
year = "2010",
month = jan,
day = "1",
doi = "10.1093/cvr/cvp275",
language = "English",
volume = "85",
pages = "155--166",
journal = "CARDIOVASC RES",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "1",

}

RIS

TY - JOUR

T1 - Endogenous generation and protective effects of nitro-fatty acids in a murine model of focal cardiac ischaemia and reperfusion

AU - Rudolph, Volker

AU - Rudolph, Tanja K

AU - Schopfer, Francisco J

AU - Bonacci, Gustavo

AU - Woodcock, Steven R

AU - Cole, Marsha P

AU - Baker, Paul R S

AU - Ramani, Ravi

AU - Freeman, Bruce A

PY - 2010/1/1

Y1 - 2010/1/1

N2 - AIMS: Nitrated fatty acids (NO(2)-FA) have been identified as endogenous anti-inflammatory signalling mediators generated by oxidative inflammatory reactions. Herein the in vivo generation of nitro-oleic acid (OA-NO(2)) and nitro-linoleic acid (LNO(2)) was measured in a murine model of myocardial ischaemia and reperfusion (I/R) and the effect of exogenous administration of OA-NO(2) on I/R injury was evaluated.METHODS AND RESULTS: In C57/BL6 mice subjected to 30 min of coronary artery ligation, endogenous OA-NO(2) and LNO(2) formation was observed after 30 min of reperfusion, whereas no NO(2)-FA were detected in sham-operated mice and mice with myocardial infarction without reperfusion. Exogenous administration of 20 nmol/g body weight OA-NO(2) during the ischaemic episode induced profound protection against I/R injury with a 46% reduction in infarct size (normalized to area at risk) and a marked preservation of left ventricular function as assessed by transthoracic echocardiography, compared with vehicle-treated mice. Administration of OA-NO(2) inhibited activation of the p65 subunit of nuclear factor kappaB (NFkappaB) in I/R tissue. Experiments using the NFkappaB inhibitor pyrrolidinedithiocarbamate also support that protection lent by OA-NO(2) was in part mediated by inhibition of NFkappaB. OA-NO(2) inhibition of NFkappaB activation was accompanied by suppression of downstream intercellular adhesion molecule 1 and monocyte chemotactic protein 1 expression, neutrophil infiltration, and myocyte apoptosis.CONCLUSION: This study reveals the de novo generation of fatty acid nitration products in vivo and reveals the anti-inflammatory and potential therapeutic actions of OA-NO(2) in myocardial I/R injury.

AB - AIMS: Nitrated fatty acids (NO(2)-FA) have been identified as endogenous anti-inflammatory signalling mediators generated by oxidative inflammatory reactions. Herein the in vivo generation of nitro-oleic acid (OA-NO(2)) and nitro-linoleic acid (LNO(2)) was measured in a murine model of myocardial ischaemia and reperfusion (I/R) and the effect of exogenous administration of OA-NO(2) on I/R injury was evaluated.METHODS AND RESULTS: In C57/BL6 mice subjected to 30 min of coronary artery ligation, endogenous OA-NO(2) and LNO(2) formation was observed after 30 min of reperfusion, whereas no NO(2)-FA were detected in sham-operated mice and mice with myocardial infarction without reperfusion. Exogenous administration of 20 nmol/g body weight OA-NO(2) during the ischaemic episode induced profound protection against I/R injury with a 46% reduction in infarct size (normalized to area at risk) and a marked preservation of left ventricular function as assessed by transthoracic echocardiography, compared with vehicle-treated mice. Administration of OA-NO(2) inhibited activation of the p65 subunit of nuclear factor kappaB (NFkappaB) in I/R tissue. Experiments using the NFkappaB inhibitor pyrrolidinedithiocarbamate also support that protection lent by OA-NO(2) was in part mediated by inhibition of NFkappaB. OA-NO(2) inhibition of NFkappaB activation was accompanied by suppression of downstream intercellular adhesion molecule 1 and monocyte chemotactic protein 1 expression, neutrophil infiltration, and myocyte apoptosis.CONCLUSION: This study reveals the de novo generation of fatty acid nitration products in vivo and reveals the anti-inflammatory and potential therapeutic actions of OA-NO(2) in myocardial I/R injury.

KW - Alkylation

KW - Animals

KW - Apoptosis

KW - Disease Models, Animal

KW - Echocardiography

KW - Fatty Acids/metabolism

KW - Inflammation/etiology

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Myocardial Ischemia/metabolism

KW - Myocardial Reperfusion Injury/prevention & control

KW - Neutrophil Infiltration

KW - Nitric Oxide/metabolism

KW - Proline/analogs & derivatives

KW - Thiocarbamates/pharmacology

KW - Transcription Factor RelA/metabolism

U2 - 10.1093/cvr/cvp275

DO - 10.1093/cvr/cvp275

M3 - SCORING: Journal article

C2 - 19666678

VL - 85

SP - 155

EP - 166

JO - CARDIOVASC RES

JF - CARDIOVASC RES

SN - 0008-6363

IS - 1

ER -