Effect and mechanism of baicalin in rats with pulmonary hypertension

AIM:To observe the effect of baicalin on rats with pulmonary hypertension induced by monocrotaline (MCT) and on pulmonary artery smooth muscle cell apoptosis. METHODS: Forty eight rats were randomly divided into control group, model group, positive drug group (simvastatin group), and baicalin groups according to three dosages (20 mg/kg, 40 mg/kg, 80 mg/kg, i.e., low, medium, high baicalin group), eight per group. Rats with pulmonary hypertension were induced by MCT, simvastatin group was given simvastatin 2 mg/kg by gavage, and baicalin groups were given baicalin (20, 40, 80 mg/kg) by gavage. The effect of baicalin on pulmonary artery pressure and the index of right ventricular hypertrophy were observed. Pulmonary artery morphology was examined by HE staining and Bcl2 and Bax changes of pulmonary vascular smooth muscle cells were detected by immunohistochemistry. RESULTS: Compared with those in the model group, high and medium baicalin reduced MCTinduced pulmonary arterial pressure (P<001), high baicalin reduced indexes of right ventricular hypertrophy (P<005), high and medium baicalin reduced the media tunica thickness and area percentage of pulmonary artery wall (P<001), and high and medium baicalin increased the positive staining rate of Bax and reduced the positive staining rate of Bcl2 (P<001) in a concentrationdependent manner. CONCLUSION: Baicalin inhibits MCTinduced pulmonary hypertension and reverses reconstruction of pulmonary artery in rats, probably by inhibiting proliferation of pulmonary artery smooth muscle cells and inducing their apoptosis.