Key result
Acacetin protected against high glucose-induced injury in vitro and improved cardiac function while reducing myocardial injury, oxidative stress, and inflammation in a rat model of diabetic cardiomyopathy.
Why the study?
Diabetic cardiomyopathy significantly impairs quality of life and can lead to heart failure, but the therapeutic effect of acacetin on diabetic cardiomyopathy was not understood.
Does acacetin improve cardiac function and reduce myocardial injury in preclinical models of diabetic cardiomyopathy?
Does acacetin improve cardiac function and reduce myocardial injury in preclinical models of diabetic cardiomyopathy?
Acacetin demonstrates cardioprotective effects in preclinical models of diabetic cardiomyopathy by inhibiting oxidative stress and energy metabolism via the PPAR-α/AMPK pathway.
No immediate clinical role; extends preclinical data but leaves open human translation in diabetic cardiomyopathy.
Diabetic cardiomyopathy seriously affects the life quality of diabetic patients and can lead to heart failure and death in severe cases. Acacetin was reported to be an anti-oxidant and anti-inflammatory agent in several cardiovascular diseases. However, the effect of acacetin on diabetic cardiomyopathy was not understood. This study was designed to explore the therapeutic effect of acacetin on diabetic cardiomyopathy and the potential mechanism with in vitro and in vivo experimental techniques. In cultured neonatal rat cardiomyocytes and H9C2 cardiac cells, acacetin (0.3, 1, 3 μM) showed effective protection against high glucose-induced injury in a concentration-dependent manner. Acacetin countered high glucose-induced increase of Bax and decrease of Bcl-2, SOD1, and SOD2. In streptozotocin-induced rat diabetic cardiomyopathy model, treatment with acacetin prodrug (10 mg/kg, s.c., b.i.d.) significantly improved the cardiac function and reduced myocardial injury, and reversed the increase of serum MDA, Ang Ⅱ, and IL-6 levels and myocardial Bax and IL-6, and the decrease of serum SOD, indicating that acacetin plays a cardioprotective effect by inhibiting oxidative stress, inflammation, and apoptosis. In addition, both in vitro and in vivo experimental results showed that acacetin increased the expression of PPAR-α and pAMPK, indicating that PPAR-α and pAMPK are potential targets of acacetin for the protection against diabetic cardiomyopathy. This study demonstrates the new application of acacetin for treating diabetic cardiomyopathy.
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Song et al. (2022) studied Diabetic cardiomyopathy. Acacetin vs. High glucose (in vitro) / untreated diabetic model (in vivo) was evaluated on Cardiac function, myocardial injury, oxidative stress, inflammation, and apoptosis markers. Acacetin protected against high glucose-induced injury in vitro and improved cardiac function while reducing myocardial injury, oxidative stress, and inflammation in a rat model of diabetic cardiomyopathy.
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