Key result
Pretreatment with GDF11 significantly improved cardiac function, decreased infarct size and oxidative stress, and increased autophagy in diabetic rats subjected to myocardial ischemia reperfusion.
Why the study?
The study was conducted to investigate whether GDF11 ameliorates myocardial ischemia reperfusion injury in diabetic rats and to explore the underlying mechanisms.
Does GDF11 pretreatment ameliorate myocardial ischemia reperfusion injury in diabetic rats?
Does GDF11 pretreatment ameliorate myocardial ischemia reperfusion injury in diabetic rats?
GDF11 provides cardioprotection against ischemia-reperfusion injury in diabetic models via antioxidant effects and autophagy up-regulation.
GDF11 may attenuate diabetic MIR in rats; leaves open clinical translation and human trials.
PURPOSE: To investigate whether GDF11 ameliorates myocardial ischemia reperfusion (MIR) injury in diabetic rats and explore the underlying mechanisms. METHODS: Diabetic and non-diabetic rats subjected to MIR (30 min of coronary artery occlusion followed by 120 min of reperfusion) with/without GDF11 pretreatment. Cardiac function, myocardial infarct size, creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), superoxide dismutase (SOD) 15-F2tisoprostane, autophagosome, LC3II/I ratio and Belcin-1 level were determined to reflect myocardial injury, oxidative stress and autophagy, respectively. In in vitro study, H9c2 cells cultured in high glucose (HG, 30mM) suffered hypoxia reoxygenation (HR) with/without GDF11, hydrogen peroxide (H2O2) and autophagy inhibitor 3-methyladenine (3-MA) treatment, cell injury; oxidative stress and autophagy were assessed. RESULTS: Pretreatment with GDF11 significantly improved cardiac morphology and function in diabetes, concomitant with decreased arrhythmia severity, infarct size, CK-MB, LDH and 15-F2tisoprostane release, increased SOD activity and autophagy level. In addition, GDF11 notably reduced HR injury in H9c2 cells with HG exposure, accompanied by oxidative stress reduction and autophagy up-regulation. However, those effects were completely reversed by H2O2 and 3-MA. CONCLUSION: GDF11 can provide protection against MIR injury in diabetic rats, and is implicated in antioxidant stress and autophagy up-regulation.
No takes yet. Share an insight, caveat, or question.
Zhou et al. (2019) studied Myocardial ischemia reperfusion injury in diabetes. GDF11 pretreatment vs. No GDF11 pretreatment was evaluated on Cardiac morphology and function, infarct size, oxidative stress, and autophagy markers. Pretreatment with GDF11 significantly improved cardiac function, decreased infarct size and oxidative stress, and increased autophagy in diabetic rats subjected to myocardial ischemia reperfusion.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: