Cardiovascular Actions

Berberine may be effective for congestive heart failure and arrhythmia as it has demonstrated positive inotropic, negative chronotropic, antiarrhythmic and vasodilator properties (Lau et al 2001).

After 8 weeks of treatment oral doses of berberine (10 mg/kg) improved cardiac Goldenseal 632

function and prevented development of left ventricular hypertrophy induced by

pressure overload In rats (Hong et al 2002, 2003). Berberlne was found to reduce left ventricular end-dlastollc pressure, Improve contraction and relaxation and decrease the amount of the atrophied heart muscle.

Berberlne has also been found to Increase cardiac output In dogs with left ventricular failure due to Ischaemla (Huang et al 1992). Over 10 days, Intravenous administration of berberine (1 mg/kg, within 3 minutes) followed by a constant infusion (0.2 mg/kg/min, 30 minutes) increased the cardiac output and decreased left ventricular end-diastolic pressure, DBP and systemic vascular resistance, but did not affect heart rate. This study shows that berberine may be able to improve impaired left ventricular function by exerting positive inotropic effects and mild systemic vasodilatation. These results, although interesting, should be evaluated cautiously as the method of administration was intravenous. The hypotensive effects of the berberine derivative, 6-protoberberine (PTB-6) were studied in spontaneously hypertensive rats (Liu et al 1999). PTB-6 lowered SBP in a dose-dependent manner (5 mg/kg :-31.1 ± 1.6 mmHg; 10 mg/kg:-42.4 ± 3.1 mmHg). The berberine derivative also reduced cardiac output and heart rate. The authors conclude that the antihypertensive effect of PTB-6 is probably caused by a central sympatholytic effect.


Berberine upregulates the LDL receptor (LDLR) by stabilising the LDLR mRNA (Abidi et al 2005, Kong et al 2004). Hamsters fed a high-fat diet for 2 weeks, followed by treatment with oral doses of berberine (100 mg/kg) for 10 days demonstrated a 40% reduction of cholesterol, including a 42% reduction in LDL-cholesterol (Kong et al 2004). No effect on HDL-cholesterol was noted.

Berberine may have potential as an anti-atherosclerotic agent because of a demonstrated inhibition of lysophosphatidylcholine (lysoPC)-induced DNA synthesis and cell proliferation in vascular smooth muscle cells (VSMCs) in vivo (Cho et al 2005). Berberine also inhibited the migration of lysoPC-stimulated VSMCs and the activity of extracellular signal-regulated kinases, reduced transcription factor AP-1 and intracellular reactive oxygen species. This suggests that berberine may be useful for the prevention of atherosclerosis.

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