Abstract
Propolis, a traditional medicine, has been widely used for a thousand years as an anti-inflammatory and antioxidant drug. The flavonoid fraction is the main active component of propolis, which possesses a wide range of biological activities, including activities related to heart disease. However, the role of the flavonoids extraction from propolis (FP) in heart disease remains unknown. This study shows that FP could attenuate ISO-induced pathological cardiac hypertrophy (PCH) and heart failure in mice. The effect of the two fetal cardiac genes, atrial natriuretic factor (ANF) and β-myosin heavy chain (β-MHC), on PCH was reversed by FP. Echocardiography analysis revealed cardiac ventricular dilation and contractile dysfunction in ISO-treated mice. This finding is consistent with the increased heart weight and cardiac ANF protein levels, massive replacement fibrosis, and myocardial apoptosis. However, pretreatment of mice with FP could attenuate cardiac dysfunction and hypertrophy in vivo. Furthermore, the cardiac protection of FP was suppressed by the pan-PI3K inhibitor wortmannin. FP is a novel cardioprotective agent that can attenuate adverse cardiac dysfunction, hypertrophy, and associated disorder, such as fibrosis. The effects may be closely correlated with PI3K/AKT signaling. FP may be clinically used to inhibit PCH progression and heart failure.
Highlights
Cardiac hypertrophy is frequently observed in various clinical conditions, including hypertension and aortic stenosis
Six of the peaks were characterized as pinocembrin, kaempferol, isosakuranetin, pinobanksin-3-O-acetate, 12-acetoxyviscidone, galangin, and chrysin by comparison to the external standards and the mass data relative abundance and fragmentation rules according to reported references [24,25,26,27] (Table 2)
FPISO cotreated mice exhibited higher p-AKT in the hearts than those treated with from propolis (FP) alone; the difference was not significant. These results indicated that the cardioprotective effect of FP could be attributed to the antihypertrophic and antiapoptotic activities, which possibly involved the PI3KAKT signaling pathway
Summary
Cardiac hypertrophy is frequently observed in various clinical conditions, including hypertension and aortic stenosis. It can progressively lead to heart failure (HF). HF is the most frequent cause of cardiovascular death worldwide. HF is caused by a pathological state that results in insufficient cardiac output [1,2,3,4,5,6]. There has been great progress in therapy, the mortality and morbidity of HF place it in the top 5 lethal diseases. The high mortality of HF imposes a significant economic burden in both China and Western countries [7]. Identifying novel preventive and/or therapeutic strategies to counteract this deadly disease is of importance
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