Berberine significantly reduced left ventricular myocardium cell size (p<0.001) and decreased whole heart and left ventricular weight in rats with pressure-overload induced cardiac hypertrophy.
Does berberine improve cardiac function and prevent left ventricular hypertrophy in rats with pressure-overload induced cardiac hypertrophy?
In a rat model of pressure-overload, berberine improved cardiac function and inhibited left ventricular hypertrophy, suggesting potential therapeutic value for heart failure.
p-value: p=<0.001
Berberine is the basic chemical component of a Chinese herb, Coptis chinensis Franch (coptis), considered to be useful in treating some diseases of the cardiovascular system, such as hypertension and chronic heart failure (CHF). In this study, we investigate the inhibitory effect of berberine on experimental cardiac hypertrophy, which is regarded as a risk factor of CHF and other heart diseases. Forty-two male SD rats were divided into four groups: age-matched control, aortic banding model, berberine-treated group and captopril-treated group. Cardiac hypertrophy was induced by suprarenal abdominal aorta constriction (banding). The drugs were orally administered for 8 weeks starting from 4 weeks after surgery at dosage of berberine 10 mg/kg and captopril 50 mg/kg. Blood pressure (BP) was measured four times during the period of the experiment, and hemodynamic parameters, cardiac index, cell size of left ventricular myocardium and total protein of left ventricular tissue were detected 8 weeks after treatment with drugs. The data from the present study showed that: (1) The BP of the aorta banded rats was increased compared with those of the normal (p < 0.001) and the age-matched control rats (p < 0.001), and berberine showed no significant effect on it. (2) After 8 weeks of treatment with berberine, the elevated left ventricular end diastolic pressure (LVEDP) was slightly decreased compared with the aortic banded rats. Meanwhile, the maximum rates of contraction and relaxation (+/- dp/dtmax) was increased (p < 0.05) and the time to reach the point of maximum rate from beginning of contraction (t-dp/dt) was shortened (p < 0.01), indicating that the functions of heart, both contraction and relaxation, were improved. (3) Cardiac growth was inhibited by treatment with berberine. Both whole heart and left ventricular weight were notably decreased compared with the banded rats (p < 0.05 and p < 0.01). (4) The cell size of left ventricular myocardium was significantly reduced (p < 0.001) and the total protein of left ventricular tissue was slightly down-regulated by treatment with berberine. These data suggest that berberine can improve abnormal cardiac function and can prevent the development of left ventricular hypertrophy induced by pressure-overload. This indicates that it may have therapeutic potential in the treatment of CHF.
Hong et al. (Tue,) conducted a other in Pressure-overload induced cardiac hypertrophy (n=42). Berberine vs. Aortic banding model (untreated), captopril (50 mg/kg), and age-matched control was evaluated on Cardiac hypertrophy (whole heart weight, left ventricular weight, and cell size of left ventricular myocardium) (p=<0.001). Berberine significantly reduced left ventricular myocardium cell size (p<0.001) and decreased whole heart and left ventricular weight in rats with pressure-overload induced cardiac hypertrophy.