scholarly journals The Role of PPARα in Metformin-Induced Attenuation of Mitochondrial Dysfunction in Acute Cardiac Ischemia/Reperfusion in Rats

2012 ◽  
Vol 13 (6) ◽  
pp. 7694-7709 ◽  
Author(s):  
Giselle Barreto-Torres ◽  
Rebecca Parodi-Rullán ◽  
Sabzali Javadov
Keyword(s):  
Mitochondrial Dysfunction ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Acute Cardiac Ischemia

scholarly journals Protective role of melatonin in cardiac ischemia-reperfusion injury: From pathogenesis to targeted therapy

2018 ◽  
Vol 64 (3) ◽  
pp. e12471 ◽  
Author(s):  
Hao Zhou ◽  
Qiang Ma ◽  
Pingjun Zhu ◽  
Jun Ren ◽  
Russel J. Reiter ◽  
...  
Keyword(s):  
Targeted Therapy ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Cardiac Ischemia

scholarly journals The cardiolipin-binding peptide elamipretide mitigates fragmentation of cristae networks following cardiac ischemia reperfusion in rats

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Mitchell E. Allen ◽  
Edward Ross Pennington ◽  
Justin B. Perry ◽  
Sahil Dadoo ◽  
Marina Makrecka-Kuka ◽  
...  
Keyword(s):  
Structure Function ◽  
Mitochondrial Dysfunction ◽  
Ischemia Reperfusion ◽  
Clinical Stage ◽  
Cardiac Ischemia ◽  
Biophysical Properties ◽  
Mitochondrial Membranes ◽  
Binding Peptide ◽  
Mitochondrial Structure ◽  
Block Face

AbstractMitochondrial dysfunction contributes to cardiac pathologies. Barriers to new therapies include an incomplete understanding of underlying molecular culprits and a lack of effective mitochondria-targeted medicines. Here, we test the hypothesis that the cardiolipin-binding peptide elamipretide, a clinical-stage compound under investigation for diseases of mitochondrial dysfunction, mitigates impairments in mitochondrial structure-function observed after rat cardiac ischemia-reperfusion. Respirometry with permeabilized ventricular fibers indicates that ischemia-reperfusion induced decrements in the activity of complexes I, II, and IV are alleviated with elamipretide. Serial block face scanning electron microscopy used to create 3D reconstructions of cristae ultrastructure reveals that disease-induced fragmentation of cristae networks are improved with elamipretide. Mass spectrometry shows elamipretide did not protect against the reduction of cardiolipin concentration after ischemia-reperfusion. Finally, elamipretide improves biophysical properties of biomimetic membranes by aggregating cardiolipin. The data suggest mitochondrial structure-function are interdependent and demonstrate elamipretide targets mitochondrial membranes to sustain cristae networks and improve bioenergetic function.

NO produced by endothelial NO synthase is a mediator of delayed preconditioning-induced endothelial protection

2003 ◽  
Vol 284 (6) ◽  
pp. H2053-H2060 ◽  
Author(s):  
Karine Laude ◽  
Julie Favre ◽  
Christian Thuillez ◽  
Vincent Richard
Keyword(s):  
Ischemia Reperfusion ◽  
No Synthase ◽  
Cardiac Ischemia ◽  
Sham Surgery ◽  
Nos Inhibitor ◽  
Coronary Endothelial Cells ◽  
Cardiac Preconditioning ◽  
Coronary Endothelium ◽  
Inos Inhibition

Preconditioning with brief periods of ischemia-reperfusion (I/R) induces a delayed protection of coronary endothelial cells against reperfusion injury. We assessed the possible role of nitric oxide (NO) produced during prolonged I/R as a mediator of this endothelial protection. Anesthetized rats were subjected to 20-min cardiac ischemia/60-min reperfusion, 24 h after sham surgery or cardiac preconditioning (1 × 2-min ischemia/5-min reperfusion and 2 × 5-min ischemia/5-min reperfusion). The nonselective NO synthase (NOS) inhibitor l-NAME, the selective inhibitors of neuronal (7-nitroindazole) or inducible (1400W) NOS, or the peroxynitrite scavenger seleno-l-methionine were administered 10 min before prolonged ischemia. Preconditioning prevented the reperfusion-induced impairment of coronary endothelium-dependent relaxations to acetylcholine (maximal relaxation: sham 77 ± 3; I/R 44 ± 6; PC 74 ± 5%). This protective effect was abolished by l-NAME (41 ± 7%), whereas 7-NI, 1400W or seleno-l-methionine had no effect. The abolition of preconditioning by l-NAME, but not by selective nNOS or iNOS inhibition, suggests that NO produced by eNOS is a mediator of delayed endothelial preconditioning.

scholarly journals The protective role of interleukin-18 binding protein in a murine model of cardiac ischemia/reperfusion injury

2015 ◽  
Vol 28 (12) ◽  
pp. 1436-1444 ◽  
Author(s):  
Haifeng Gu ◽  
Minghua Xie ◽  
Liqian Xu ◽  
Xiaojun Zheng ◽  
Yunmei Yang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Murine Model ◽  
Ischemia Reperfusion Injury ◽  
Binding Protein ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Cardiac Ischemia ◽  
Interleukin 18

scholarly journals N-acetylcysteine with low-dose estrogen reduces cardiac ischemia-reperfusion injury

2019 ◽  
Vol 242 (2) ◽  
pp. 37-50 ◽  
Author(s):  
Sivaporn Sivasinprasasn ◽  
Siripong Palee ◽  
Kenneth Chattipakorn ◽  
Thidarat Jaiwongkum ◽  
Nattayaporn Apaijai ◽  
...  
Keyword(s):  
Infarct Size ◽  
Mitochondrial Dysfunction ◽  
Low Dose ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Coronary Artery Ligation ◽  
Sham Operation ◽  
Myocardial Infarct Size ◽  
Ovx Rats ◽  
Cardiometabolic Function

Myocardial damage and mitochondrial dysfunction caused by cardiac ischemia-reperfusion (I/R) injury are intensified by endogenous estrogen deprivation. Although N-acetylcysteine (NAC) exerted cardioprotective effects, its benefits when used in combination with hormone therapy are unknown. We tested the hypothesis that a combination of NAC with low-dose estrogen improves cardiometabolic function and protects cardiac mitochondria against I/R injury, to a similar extent to regular-dose estrogen treatment, in estrogen-deprived rats. Female Wistar rats had a bilateral ovariectomy (OVX) or sham operation. Twelve weeks after the operation, OVX rats were treated with regular-dose estrogen (E; 50 µg/kg/day), low-dose estrogen (e; 25 µg/kg/day), NAC (N; 100 mg/kg/day) or combined low-dose estradiol with NAC (eN) for 4 weeks (n = 6/group). Metabolic parameters, echocardiography, heart rate variability and then cardiac I/R protocol involving 30-min coronary artery ligation, followed by 120-min reperfusion, were performed. OVX rats had increased body weight, visceral fat, fasting plasma glucose, HOMA-IR index, triglycerides, cholesterol and LDL levels (P < 0.05 vs sham). Only OVX-E and OVX-eN had a similarly improved HOMA-IR index. LVEF was increased in all treatment groups, but HRV was restored only by OVX-E and OVX-eN. After I/R, myocardial infarct size was decreased in both OVX-E and OVX-eN groups. OVX-E and OVX-eN rats similarly had a reduced mitochondrial ROS level and increased mitochondrial membrane potential in the ischemic myocardium. In conclusion, combined NAC with low-dose estrogen and regular-dose estrogen therapy similarly improve cardiometabolic function, prevent cardiac mitochondrial dysfunction and reduces the infarct size in estrogen-deprived rats with cardiac I/R injury.

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