Fig. 7
ENOblock reverses hypoxia-induced PH in mice. a A diagrammatic sketch depicts the hypoxia-induced PH mice model and ENOblock treatment protocol (n = 8–10 per group). C57BL/6 J mice were exposed to normoxia or hypoxia (10% O2) for 2 weeks before the ENOblock treatment. During the treatment period, the mice were continuously exposed to normoxia or hypoxia and received 0.5 mg/day/mouse ENOblock treatment via intraperitoneal injection for 2 weeks (one injection per day in the first week and one injection every other day in the second week). After the ENOblock treatment, we analyzed and calculated RVSP c (n = 8–10 per group, **P < 0.01), right ventricular hypertrophy d (n = 8–10 per group, **P < 0.01), and pulmonary artery remodeling e (**P < 0.01). The representative tracings of RVP are shown in b and the representative pulmonary artery images (HE staining) in the lung sections of experimental mice are shown in f (Scale bars, 50 μm). g The lung sections of mice from each group were co-immunostained with SMA and Ki67 antibodies and DAPI (Scale bars, 50 μm). The white arrows indicate the proliferating PASMC and h the proliferation rates of PASMCs were quantified in each group. Data represent the mean ± SEM. Student t test and one-way ANOVA were used to compare two and multiple groups. Bonferroni post-tests were carried out after ANOVA
