Preconditioning prevents loss in mitochondrial function and release of cytochrome c during prolonged cardiac ischemia/reperfusion

2006 ◽  
Vol 453 (1) ◽  
pp. 130-134 ◽  
Author(s):  
Kathleen C. Lundberg ◽  
Luke I. Szweda
Keyword(s):  
Cytochrome C ◽  
Mitochondrial Function ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia

scholarly journals Inhibiting miR-205 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Function, and Apoptosis

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Yuerong Xu ◽  
Wangang Guo ◽  
Di Zeng ◽  
Yexian Fang ◽  
Runze Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Function ◽  
Infarct Size ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Myocardial Infarct Size ◽  
Neonatal Cardiomyocytes

Background. miR-205 is important for oxidative stress, mitochondrial dysfunction, and apoptosis. The roles of miR-205 in cardiac ischemia/reperfusion (I/R) injury remain unknown. The aim of this research is to reveal whether miR-205 could regulate cardiac I/R injury by focusing upon the oxidative stress, mitochondrial function, and apoptosis. Methods. Levels of miR-205 and Rnd3 were examined in the hearts with I/R injury. Myocardial infarct size, cardiac function, oxidative stress, mitochondria function, and cardiomyocyte apoptosis were detected in mice with myocardial ischemia/reperfusion (MI/R) injury. The primary neonatal cardiomyocytes underwent hypoxia/reoxygenation (H/R) to simulate MI/R injury. Results. miR-205 levels were significantly elevated in cardiac tissues from I/R in comparison with those from Sham. In comparison with controls, levels of Rnd3 were significantly decreased in the hearts from mice with MI/R injury. Furthermore, inhibiting miR-205 alleviated MI/R-induced apoptosis, reduced infarct size, prevented oxidative stress increase and mitochondrial fragmentation, and improved mitochondrial functional capacity and cardiac function. Consistently, overexpression of miR-205 increased infarct size and promoted apoptosis, oxidative stress, and mitochondrial dysfunction in mice with MI/R injury. In cultured mouse neonatal cardiomyocytes, downregulation of miR-205 reduced oxidative stress in H/R-treated cardiomyocytes. Finally, inhibiting Rnd3 ablated the cardioprotective effects of miR-205 inhibitor in MI/R injury. Conclusions. We conclude that inhibiting miR-205 reduces infarct size, improves cardiac function, and suppresses oxidative stress, mitochondrial dysfunction, and apoptosis by promoting Rnd3 in MI/R injury. miR-205 inhibitor-induced Rnd3 activation is a valid target to treat MI/R injury.

Cardiac ischemia/reperfusion, aging, and redox-dependent alterations in mitochondrial function

2003 ◽  
Vol 420 (2) ◽  
pp. 201-208 ◽  
Author(s):  
Hesham A Sadek ◽  
Amy C Nulton-Persson ◽  
Pamela A Szweda ◽  
Luke I Szweda
Keyword(s):  
Mitochondrial Function ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia

Mitochondrial function in response to cardiac ischemia-reperfusion after oral treatment with quercetin

2002 ◽  
Vol 32 (11) ◽  
pp. 1220-1228 ◽  
Author(s):  
Paul S Brookes ◽  
Stanley B Digerness ◽  
Dale A Parks ◽  
Victor Darley-Usmar
Keyword(s):  
Mitochondrial Function ◽  
Ischemia Reperfusion ◽  
Oral Treatment ◽  
Cardiac Ischemia

CELASTROL FAMILY HSP90 INHIBITORS IMPROVE MITOCHONDRIAL FUNCTION IN A CARDIAC ISCHEMIA/REPERFUSION IN VITRO MODEL

2020 ◽  
Vol 36 (10) ◽  
pp. S8
Author(s):  
H. Aceros ◽  
K. Khalil ◽  
M. Borie ◽  
M. Tanase ◽  
S. Der Sarkissian ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
In Vitro Model ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Hsp90 Inhibitors ◽  
Vitro Model

scholarly journals 406-1 Hypoxia regulatable Aav-2 vector protects against cardiac ischemia/reperfusion injury

2004 ◽  
Vol 43 (5) ◽  
pp. A533
Author(s):  
Alok S Pachori ◽  
Luis G Melo ◽  
Lunan Zhang ◽  
Richard E Pratt ◽  
Victor J Dzau
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia

Schisandrin Restores the Amyloid β-Induced Impairments on Mitochondrial Function, Energy Metabolism, Biogenesis, and Dynamics in Rat Primary Hippocampal Neurons

Pharmacology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Zhongyuan Piao ◽  
Lin Song ◽  
Lifen Yao ◽  
Limei Zhang ◽  
Yichan Lu
Keyword(s):  
Energy Metabolism ◽  
Cytochrome C ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Citrate Synthase ◽  
Mitochondrial Permeability Transition ◽  
Amyloid Β ◽  
Mitochondrial Functions ◽  
Primary Hippocampal Neurons

Introduction: Schisandrin which is derived from Schisandra chinensis has shown multiple pharmacological effects on various diseases including Alzheimer’s disease (AD). It is demonstrated that mitochondrial dysfunction plays an essential role in the pathogenesis of neurodegenerative disorders. Objective: Our study aims to investigate the effects of schisandrin on mitochondrial functions and metabolisms in primary hippocampal neurons. Methods: In our study, rat primary hippocampal neurons were isolated and treated with indicated dose of amyloid β1–42 (Aβ1–42) oligomer to establish a cell model of AD in vitro. Schisandrin (2 μg/mL) was further subjected to test its effects on mitochondrial function, energy metabolism, mitochondrial biogenesis, and dynamics in the Aβ1–42 oligomer-treated neurons. Results and Conclusions: Our findings indicated that schisandrin significantly alleviated the Aβ1–42 oligomer-induced loss of mitochondrial membrane potential and impaired cytochrome c oxidase activity. Additionally, the opening of mitochondrial permeability transition pore and release of cytochrome c were highly restricted with schisandrin treatment. Alterations in cell viability, ATP production, citrate synthase activity, and the expressions of glycolysis-related enzymes demonstrated the relief of defective energy metabolism in Aβ-treated neurons after the treatment of schisandrin. For mitochondrial biogenesis, elevated expression of peroxisome proliferator-activated receptor γ coactivator along with promoted mitochondrial mass was found in schisandrin-treated cells. The imbalance in the cycle of fusion and fission was also remarkably restored by schisandrin. In summary, this study provides novel mechanisms for the protective effect of schisandrin on mitochondria-related functions.

Sign in / Sign up

Export Citation Format

Share Document