Key result
Paeonol administration at 200 mg/kg significantly improved left ventricular ejection fraction to 78.9% compared to 69.1% in diabetic controls, while reducing myocardial apoptosis and fibrosis.
Why the study?
Does paeonol improve cardiac function and reduce myocardial injury in a rat model of diabetic cardiomyopathy?
Does paeonol improve cardiac function and reduce myocardial injury in a rat model of diabetic cardiomyopathy?
Absolute Event Rate: 78.9% vs 69.1%
p-value: p=<0.05
In a rat model of diabetic cardiomyopathy, paeonol attenuated cardiac dysfunction, apoptosis, and fibrosis by modulating PI3K/Akt-GSK-3β signaling and reducing inflammatory mediators.
Paeonol may benefit diabetic cardiomyopathy in animals; leaves open human translation and requires clinical trials.
The present study was taken as an effort to assess the effects of paeonol on diabetic cardiomyopathy. Diabetes was induced in separate groups of Sprague-Dawley rats using streptozotocin. Treatment group animals received paeonol (50, 100 or 200 mg/kg body weight/day; orally) 5 weeks after streptozotocin induction for 6 weeks. Paeonol strikingly reduced myocardial apoptosis and improved cardiac function and myocardial architecture. Serum levels of glucose, reactive oxygen species and inflammatory mediators (TNF-α, IL-6 and IL-1β) were significantly reduced with decreased accumulation of collagen in the cardiac tissue. Paeonol modulated p-Akt, glycogen synthase kinase-3β and glycogen synthase, while significantly down-regulated protease-activated receptor-1, caspase-3, TNF-α, NF-κB p65, and p-Iκ-Bα expressions. Paeonol effectively suppressed diabetic cardiomyopathy by improving myocardial function, regulating the inflammatory responses and Akt signalling.
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Li et al. (2015) studied Diabetic cardiomyopathy (n=30). Paeonol vs. Diabetic control (no paeonol) was evaluated on Left ventricular ejection fraction (LVEF) (p=<0.05). Paeonol administration at 200 mg/kg significantly improved left ventricular ejection fraction to 78.9% compared to 69.1% in diabetic controls, while reducing myocardial apoptosis and fibrosis.
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