OBJECTIVETo investigate the effect of ursolic acid (UA) on the alloxan-induced myocardial fibrosis in mice and discuss the possible mechanism.

METHODSDiabetes was produced by a single injection of alloxan (70 mg/kg, i.v.) in mice. The mice were randomly divided into four groups: normal control group, model group, ursolic acid group (UA, 35 mg/kg, p.o.) and benazepril group (5 mg/kg, p. o.), and continuous administrated for 8 weeks. The blood glucose was measured 24 hours after the last administration. Detected the specific biochemical of myocardial tissue: superoxide dismutase (SOD), malondialdehyde (MDA) and hydroxyproline(HYP). Using masson staining to observe the morphology of the myocardial tissue. Immunohistochemistry was employed to determine the protein levels of TGF-beta1.

RESULTSCompared to normal group, the blood glucose, heart index, myocardial tissue MDA, HYP level were increased, and SOD activities were decreased in the diabetic mice, Masson stain showed that myocardial cells disarranged, myocardial collagen fibrosis hyperplasia. Meanwhile, the protein expression of TGF-beta1 was increased in model group. The UA group improved all the above significantly.

CONCLUSIONUA improves the myocardial collagen fibrosis in diabetic mice induced by alloxan, its mechanism may be related to inhibiting the expression of TGF-beta1 and antioxidation.