| Abstract: | Previous studies have shown that baicalin can attenuate pulmonary arterial hypertension and right ventricular hypertrophy. However, the potential mechanism remains unexplored. Nuclear factor-κB (NF-κB) and bone morphogenetic protein (BMP) signaling pathway play an important role in monocrotaline (MCT) induced pulmonary arterial hypertension (PAH). Therefore, we aimed to observe the regulation of baicalin on the NF-κB-BMP axis and the subsequent anti-proliferation in pulmonary vascular. Our results showed that baicalin could significantly decrease right ventricular systolic pressure (RVSP) and the RV/left ventricle plus septum ratio (P < 0.05), and attenuate vascular remodeling. Furthermore, the result of westen blot showed that the protein expression level of BMP receptor 2 (BMPR2) was significantly increased, while NF-κB p65, p-NF-κB p65, inhibitor of NF-κB (I-κBα) and the BMP antagonist, gremlin 1 were significantly down-regulated in the baicalin group (P < 0.05). On the other hand, the result of immunohistochemical staining in lung showed that the capillary density of pulmonary arterioles significantly increased in the baicalin group compared with the MCT group (P < 0.05). We concluded thatbaicalin exerted the protective effects against the lung and heart damagethrough inhibiting NF-κB-BMP signaling pathway, providing new mechanistic information about PAH and right ventricular hypertrophy. |
