The protective of baicalin on pulmonary hypertension vascular remodeling through regulation of TNF-α signaling pathway

Abstract

Background: Pulmonary hypertension (PH) is a life-threatening disease, so far no effective method for it. Baicalin can attenuate pulmonary artery pressure and reduce right ventricular hypertrophy in PH, however, the potential mechanism remains unexplored. Therefore, the main aim of the present study was to investigate the protective effect and of baicalin on experimental PH vascular remodeling, and reveal the underlying mechanism.Methods: Monocrotaline (MCT)-induced PH rats models was established, and baicalin was given by intragastric administration. Six weeks later, right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVHI) were recorded, lung tissue hematoxylin-eosin (H&E) staining was analysis to reveal the effect of baicalin on MCT-induced PH. In Vitro, we established TNF-α induced pulmonary artery smooth muscle cells (PASMCs) to detect the inhibition of baicalin on vascular remodeling. Furthermore, quantitative real-time polymerase chain reaction (qRT-PCR), western blot and immunofluorescence were used to detect the mRNA and protein expressions.Results: Our results indicated that baicalin could significantly attenuate MCT induced the RVSP and the right ventricular hypertrophy index (RVHI); inhibit pulmonary vascular remodeling and lung fibrosis. Moreover, our results showed baicalin could significantly decrease the expression of inflammatory cytokines, but increase the protein expression of bone morphogenetic protein type II receptor (BMPR2), ID1 and Smad1//5/8.Conclusion:Taken together, our present study confirmed the mechanism of baicalin against PH was associated with inhibition of TNF-α signaling pathway.