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Induction and Assessment of Ischemia-reperfusion Injury in Langendorff-perfused Rat Hearts
Published on: July 27, 2015
[Ischemic postconditioning attenuates ischemia/reperfusion injury in isolated hypertrophied rat heart]
Long-yun Peng1, Hong Ma, Jian-gui He
1Cardiovascular Research Institute of Sun Yat-sen University, Department of Cardiovascular Medicine, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.
Insights
Ischemic postconditioning protects hypertrophied rat hearts from injury by improving blood flow and reducing damage. This effect is partly mediated by the PI3K/Akt/GSK-3beta signaling pathway.
Area of Science:
- Cardiology
- Physiology
- Molecular Biology
Background:
- Ischemia/reperfusion injury poses a significant threat to cardiac health, particularly in hypertrophied hearts.
- Understanding protective mechanisms is crucial for developing therapeutic strategies against heart damage.
Purpose of the Study:
- To investigate the protective effects of ischemic postconditioning on ischemia/reperfusion injury in isolated hypertrophied rat hearts.
- To elucidate the role of the PI3K/Akt/GSK-3beta signaling pathway in mediating these protective effects.
Main Methods:
- A rat model of cardiac hypertrophy was established, followed by an isolated heart ischemia/reperfusion model using the Langendorff technique.
- Ischemic postconditioning was applied, and its effects on cardiac function, infarct size, and key signaling molecules (p-Akt, p-GSK-3beta) were assessed.
- The role of the PI3K/Akt/GSK-3beta pathway was further examined using the PI3K inhibitor wortmannin.
Main Results:
- Ischemic postconditioning significantly improved left ventricular systolic pressure and coronary artery flow while reducing myocardial infarction size and the release of cardiac enzymes (CPK, LDH).
- Levels of phospho-protein kinase B/Akt (Ser473) and phospho-glycogen synthase kinase-3beta (Ser9) were elevated following ischemic postconditioning.
- Wortmannin partially inhibited the protective effects of ischemic postconditioning, indicating a role for the PI3K/Akt/GSK-3beta pathway.
Conclusions:
- Ischemic postconditioning demonstrates significant cardioprotective effects against ischemia/reperfusion injury in hypertrophied rat hearts.
- The PI3K/Akt/GSK-3beta signaling pathway is partially involved in mediating the cardioprotective benefits of ischemic postconditioning.
Objective:
To explore the effects of ischemic postconditioning on ischemia/reperfusion injury in isolated hypertrophied rat heart and investigate the signal transduction pathway changes induced by ischemia postconditioning.
Methods:
Cardiac hypertrophy was induced in rats by abdominal aortic banding, and isolated hypertrophied rat heart ischemia/reperfusion model was made by Langendorff technique to evaluate the effects of ischemia postconditioning on left ventricular systole pressure, coronary artery flow, creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) release, myocardial infarction size, and the level of myocardial phospho-protein kinase B/Akt (Ser473), phospho-glycogen synthase kinase-3beta (Ser9). Following groups were studied (n = 12 each group): IR, 30 min ischemia (I)/60 min Reperfusion (R); Post: 30 min ischemia, 6 circles of 10 s I/10 s R followed by 60 min R; Post Wort: 30 min ischemia, 6 circles of 10 s I/10 s R, wortmannin (10(-7) mol/L) followed by 60 min R; Wort: 30 min ischemia, wortmannin (10(-7) mol/L) followed by 60 min R.
Results:
Left ventricular systolic pressure and coronary artery flow were significantly increased, myocardial infarction size and the release of CPK, LDH significantly reduced in Post group compared to that in IR group. Phospho-protein kinase B/Akt (Ser473) and phospho-glycogen synthase kinase-3beta (Ser9) levels were also significantly higher in Post group than that in IR group. Phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin prevented the increase of phospho-protein kinase B/Akt (Ser473) and phospho-glycogen synthase kinase-3beta (Ser9) induced by ischemic postconditioning, but only partly abolished the cardioprotection of ischemic postconditioning.
Conclusion:
Ischemic postconditioning attenuates ischemia/reperfusion injury in isolated hypertrophied rat heart. The cardioprotective effects of ischemic postconditioning were partly mediated through PI3K/Akt/GSK-3beta signaling pathway.
