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Updated: May 5, 2026
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Hyperglycemia-induced inhibition of DJ-1 expression compromised the effectiveness of ischemic postconditioning
Min Liu1, Bin Zhou, Zhong-Yuan Xia
1Department of Anesthesiology, Renmin Hospital of Wuhan University, 99 Zi Yang Road, Wuhan, Hubei 430060, China.
Abstract:
Ischemia postconditioning (IpostC) is an effective way to alleviate ischemia and reperfusion injury; however, the protective effects seem to be impaired in candidates with diabetes mellitus. To gain deep insight into this phenomenon, we explored the role of DJ-1, a novel oncogene, that may exhibit powerful antioxidant capacity in postconditioning cardioprotection in a rat model of myocardial ischemia reperfusion injury. Compared with normal group, cardiac DJ-1 was downregulated in diabetes. Larger postischemic infarct size as well as exaggeration of oxidative stress was observed, while IpostC reversed the above changes in normal but not in diabetic rats. DJ-1 was increased after ischemia and postconditioning contributed to a further elevation; however, no alteration of DJ-1 was documented in all subgroups of diabetic rats. Alteration of the cardioprotective PI3K/Akt signaling proteins may be responsible for the ineffectiveness of postconditioning in diabetes. There is a positive correlation relationship between p-Akt and DJ-1 but a negative correlation between infarct size and DJ-1, which may partially explain the interaction of DJ-1 and IpostC cardioprotection. Our result indicates a beneficial role of DJ-1 in myocardial ischemia reperfusion. Downregulation of cardiac DJ-1 may be responsible for the compromised diabetic heart responsiveness to IpostC cardioprotection.
Insights
Ischemia postconditioning (IpostC) protects hearts from injury, but diabetes impairs this effect. Downregulation of DJ-1 in diabetic hearts may explain why IpostC fails to protect against myocardial ischemia reperfusion injury.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Ischemia postconditioning (IpostC) effectively mitigates ischemia-reperfusion injury.
- Diabetic mellitus impairs the cardioprotective efficacy of IpostC.
- DJ-1, a protein with antioxidant properties, is investigated for its role in IpostC.
Purpose of the Study:
- To investigate the role of DJ-1 in IpostC cardioprotection in a rat model of myocardial ischemia reperfusion injury.
- To explore the impact of diabetes on DJ-1 expression and its relationship with IpostC efficacy.
Main Methods:
- A rat model of myocardial ischemia reperfusion injury was utilized.
- Cardiac DJ-1 levels were assessed in normal and diabetic rats.
- The effects of IpostC on infarct size, oxidative stress, and PI3K/Akt signaling were evaluated.
Main Results:
- Cardiac DJ-1 was downregulated in diabetic rats compared to normal rats.
- IpostC reduced infarct size and oxidative stress in normal rats but not in diabetic rats.
- DJ-1 levels increased post-ischemia and with IpostC in normal rats, but remained unchanged in diabetic rats.
- PI3K/Akt signaling alterations may contribute to IpostC ineffectiveness in diabetes.
- Positive correlation between p-Akt and DJ-1, and negative correlation between infarct size and DJ-1 were observed.
Conclusions:
- DJ-1 plays a beneficial role in myocardial ischemia reperfusion.
- Downregulation of cardiac DJ-1 in diabetes compromises the heart's responsiveness to IpostC cardioprotection.
- Restoring DJ-1 levels may be a therapeutic strategy to improve IpostC efficacy in diabetic patients.
