HGF Reduces Disease Severity and Inflammation by Attenuating the NF-κB Signaling in a Rat Model of Pulmonary Artery Hypertension

The purpose of the present study was to investigate the anti-inflammatory effect of hepatocyte growth factor (HGF) on pulmonary artery hypertension (PAH) in a rat model and underlying mechanisms. Wistar rats were treated with monocrotaline intravenously to induce PAH and then treated with vehicle or HGF for 2 weeks, respectively. The mean pulmonary artery pressure (mPAP), the index of right heart ventricular hypertrophy (RHVI), pathological changes, and inflammation in the lungs of individual rats were measured. The levels of serum inflammatory interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and high mobility group protein B1 (HMGB1) and the relative levels of IκBα and NF-κB p65 expression in the lungs of individual rats were determined by methods of enzyme-linked immunosorbent assay (ELISA) and Western blot. The levels of mPAP and RVHI in the HGF group were significantly lower than that in the PAH group (P < 0.05), but remained significantly higher than that of the control group (P < 0.05). Similar patterns of inflammatory scores and the levels of serum IL-6, TNF-α, ICAM-1, and HMGB1 were detected among the different groups of rats. Furthermore, the relative levels of IκBα expression in the lungs of the HGF group of rats were significantly higher than that in the control group, which were significantly higher than that in the PAH group. In contrast, the relative levels of NF-kB p65 expression in the HGF group were significantly lower than that in the PAH group (P < 0.05). HGF treatment significantly mitigated the severity of PAH and inhibited inflammation by attenuating the NF-kB signaling in the lungs of PAH rats.