Inhibiting Cytochrome C Oxidase Leads to Alleviated Ischemia Reperfusion Injury
Korean Circulation Journal
;
: 193-200, 2017.
Article
in English
| WPRIM
| ID: wpr-59345
ABSTRACT
BACKGROUND AND OBJECTIVES:
The overall purpose of this study was to investigate the role of cytochrome C oxidase (CcO) in preventing ischemia reperfusion-induced cardiac injury through gaseous signaling molecule pathways. MATERIALS ANDMETHODS:
We used CcO inhibitor, potassium cyanide (KCN) to mimic the pre-treatment of gaseous signaling molecules in a global ischemia/reperfusion (IR) injury model in rats. Intracellular reactive oxygen species (ROS) was determined by measuring mitochondrial H2O2 and mitochondrial complex activity.RESULTS:
KCN pre-treatment led to decreased infarction area after IR injury and improved cardiac function. KCN pre-treated group challenged with IR injury was associated with reduced ROS production through inhibition of activity and not downregulation of CcO expression. In addition, KCN pre-treatment was associated with enhanced expression and activity of mitochondrial antioxidase, suggesting the role of CcO in regulating IR injury through oxidative stress.CONCLUSION:
KCN pre-treatment reduced the severity of IR injury. The potential mechanism could be increased endogenous anti-oxidase activity and consequently, the enhanced clearance of ROS.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Potassium Cyanide
/
Reperfusion Injury
/
Down-Regulation
/
Reactive Oxygen Species
/
Electron Transport Complex IV
/
Oxidative Stress
/
Cytochromes
/
Cytochromes c
/
Infarction
/
Ischemia
Limits:
Animals
Language:
English
Journal:
Korean Circulation Journal
Year:
2017
Type:
Article
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