Baicalein inhibits monocrotaline-induced vascular wall thickening in rats with pulmonary hypertension

AIM:To investigate the effects of baicalein on pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT) in rats, and its molecular mechanism was further explored. METHODS:Male SD rats (n=28) were randomly divided into 4 groups:control group, MCT group, MCT+baicalein 50 mg/kg group and MCT+baicalein 100 mg/kg group. The PAH model was established by subcutaneous injection of MCT. After 2 weeks of modeling, the rats in baicalein treatment groups were gavaged baicalein 50 and 100 mg·kg^-1·d^-1 for 14 d, the rats in control group were administered with saline. After 4 weeks of modeling, right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI) and right ventricular mass index (RVMI) were detected. Masson staining was used to detect the degree of lung fibrosis. The pathomorphological changes of the pulmonary vessels were observed by HE staining. Western blot was used to detect the expression of α-smooth muscle actin (α-SMA) in the lung tissue and the phosphorylation p38, ERK and JNK in the artery. RESULTS:Compared with the control group, RVSP, RVHI and RVMI increased significantly in the MCT group (P<0.01). Pulmonary fibrosis and the thickening of pulmonary artery wall were observed. α-SMA was up-regulated and p38, ERK and JNK was activated significantly (P<0.01). Compared with the MCT group, baicalein (50 and 100 mg/kg) significantly decreased the RVSP, RVHI and RVMI (P<0.01). Lung fibrosis was reduced and the vascular wall thickening was decreased in baicalein-treated groups. Baicalein (50 and 100 mg/kg) inhibited the phosphorylation of p38, ERK and JNK compared with the MCT group (P<0.01). CONCLUSION:Baicalein ameliorates MCT-induced PAH by the inhibition of pulmonary artery wall thickening at least partially via MAPK signaling pathway.