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Exendin-4 attenuates myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein
Gangying Hu, Yijie Zhang, Hong Jiang
1Department of Cardiology, Renmin Hospital of Wuhan University; Cardiovascular Research Institute of Wuhan University, Wuhan, China Department of Cardiology, Huangshi Central Hospital, Afilliated Hospital of Hubei Polytechnic University, Huangshi, China. huxrwurm@163.com.
Insights
Exendin-4 (Ex-4) protects against myocardial ischemia-reperfusion (I/R) injury in rats by inhibiting High mobility group box 1 (HMGB1) expression. This protective effect is mediated through the glucagon-like peptide-1 receptor.
Area of Science:
- Cardiovascular Research
- Molecular Medicine
- Pharmacology
Background:
- Myocardial ischemia-reperfusion (I/R) injury is a significant clinical concern.
- High mobility group box 1 protein (HMGB1) is implicated in the pathogenesis of I/R injury.
- Exendin-4 (Ex-4), a glucagon-like peptide-1 receptor agonist, shows potential in mitigating I/R injury.
Purpose of the Study:
- To investigate the protective mechanisms of Ex-4 against myocardial I/R injury in a rat model.
- To determine the role of HMGB1 in the cardioprotective effects of Ex-4.
Main Methods:
- Male rats were treated with Ex-4 before inducing myocardial ischemia (30 min) and reperfusion (4 h).
- The effect of exendin (9-39), a glucagon-like peptide-1 receptor antagonist, was evaluated.
- Infarct size, cardiac enzyme levels (LDH, CK), oxidative stress markers (MDA, SOD), and HMGB1 expression were assessed.
Main Results:
- Ex-4 significantly reduced infarct size, LDH, and CK levels post-I/R.
- Ex-4 inhibited oxidative stress by decreasing MDA and increasing SOD activity.
- Ex-4 treatment suppressed HMGB1 expression induced by I/R.
- The protective effects of Ex-4 were abolished by exendin (9-39).
Conclusions:
- Exendin-4 attenuates myocardial I/R injury in rats.
- The cardioprotective effects of Ex-4 are associated with the inhibition of HMGB1 expression.
- These effects are mediated via the glucagon-like peptide-1 receptor.
Background:
High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia and reperfusion (I/R) injury. Exendin-4 (Ex-4), glucagon-like peptide-1 receptor agonist, has been reported to attenuate myocardial I/R injury. This study was to investigate the potential mechanism by which Ex-4 attenuates myocardial I/R injury in rats.
Methods:
Anesthetized male rats were once treated with Ex-4 (5 μg/kg, i.v.) 1 h before ischemiain the absence and/or presence of exendin (9-39) (an antagonist for glucagon-like peptide-1 receptor, 5 μg/kg, i.v.), and then subjected to ischemia for 30 min followed by reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) activity and infarct size were measured. HMGB1 expression was assessed by immunoblotting.
Results:
The results showed that pretreatment of Ex-4 could significantly decrease the infarct size and the levels of LDH and CK after 4 h reperfusion (all p < 0.05). Ex-4 could also significantly inhibit the increase of the MDA level, the decrease of the SOD level (both p < 0.05). Meanwhile, Ex-4 could significantly inhibit HMGB1 expression induced by I/R. Administration of exendin (9-39) could abolish the protective effect of Ex-4 (all p < 0.05).
Conclusions:
The present study suggested that Ex-4 could attenuate myocardial I/R injury which may be associated with inhibiting HMGB1 expression.
