Endogenous generation and protective effects of nitro-fatty acids in a murine model of focal cardiac ischaemia and reperfusion
Open accessAbstract
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.
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NO2-FAs exert pleiotropic post-translational, anti-oxidant and anti-inflammatory effects that include inhibition of vascular smooth muscle proliferation and neointima formation after injury, cardioprotection, improved endothelial function, and activation of downstream NO signaling pathways.
“NO2-FAs exert pleiotropic post-translational, anti-oxidant and anti-inflammatory effects[105,321,385] that include inhibition of vascular smooth muscle proliferation and neointima formation after injury, cardioprotection, improved endothelial function[94,386–390], and activation of downstream NO signaling pathways[385,389,391–394].”
From Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health (2017) · cites this paper as [388]
The biological mechanisms accounting for fatty acid nitration and the specific structural characteristics of products remain to be defined.
“The biological mechanisms accounting for fatty acid nitration and the specific structural characteristics of products remain to be defined.”
From Conjugated linoleic acid is a preferential substrate for fatty acid nitration (2012) · cites this paper as [17]
Conjugated linoleic acid (CLA) is a preferential substrate for nitration reactions mediated by mitochondria, digestion, and macrophage activation and following metabolic stress such as focal cardiac ischemia-reperfusion.
“The conjugated diene-containing fatty acid CLA is a preferential substrate for nitration reactions mediated by mitochondria, digestion, and macrophage activation and following metabolic stress such as focal cardiac I/R (supplemental Fig. 5) (17).”
From Conjugated linoleic acid is a preferential substrate for fatty acid nitration (2012) · cites this paper as [17]
Fatty acid nitroalkene administration protects against ischemia-reperfusion injury.
“Thus, in murine models of metabolic and inflammatory injury, fatty acid nitroalkene administration at nanomolar concentrations prevents restenosis after vessel injury (49), limits weight gain and loss of insulin sensitivity in murine models of metabolic syndrome (14), protects against ischemia-reperfusion injury (17,47,50), reduces plaque formation in a rodent model of atherosclerosis (51), and in”
From Conjugated linoleic acid is a preferential substrate for fatty acid nitration (2012) · cites this paper as [17]
Electrophilic lipids present in plants, generated by digestion of plant lipids, produced by oxidative inflammatory reactions or administered as pure synthetic homologs can regulate metabolism and the resolution of inflammatory processes.
“Consequently, electrophilic lipids which are present in plants, generated by digestion of plant lipids, produced by oxidative inflammatory reactions or administered as pure synthetic homologs [24], [26], [47], [56], can regulate metabolism and the resolution of inflammatory processes.”
From Olives and olive oil are sources of electrophilic fatty acid nitroalkenes (2014) · cites this paper as [26]
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- Authors
- 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.
- Affiliations
- Universität Hamburg (DE)
- University of Pittsburgh (US)
- ORCID
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-08-07
- Volume
- 85
- Issue
- 1
- Pages
- 155-166
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- PMC
- PMC2791055
- OpenAlex
- W2164476520
- Cited by
- 188
- References
- 39
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 6 · 2023: 9 · 2022: 5 · 2021: 11 · 2020: 13 · 2019: 14 · 2018: 16 · 2017: 11 · 2016: 16 · 2015: 15 · 2014: 10 · 2013: 12 · 2012: 11
- FWCI
- 8.95
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cardiovascular Research (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- American Heart Association
- Deutsche Forschungsgemeinschaft
- Deutsche Herzstiftung
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL64937, R01HL064937, R37HL058115, R01HL058115, R01-HL-58115)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Keywords
- nitro-fatty acids, nitro-oleic acid, myocardial ischemia-reperfusion injury, NF-κB, anti-inflammatory signaling, infarct size, left ventricular function, neutrophil infiltration, myocyte apoptosis, ICAM-1, MCP-1, pyrrolidine dithiocarbamate, cardioprotection
- MeSH terms
- Alkylation, Animals, Disease Models, Animal, Echocardiography, Fatty Acids, Inflammation, Male, Mice, Inbred C57BL, Nitric Oxide, Proline, Thiocarbamates, Myocardial Reperfusion Injury, Myocardial Ischemia, Apoptosis, Neutrophil Infiltration, Mice, Transcription Factor RelA
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