Furthermore, the MCT-treated rats showed increased HDAC activity compared with the control group (9.52 ± 0.35 RFU/μg versus 3.62 ± 0.25 RFU/μg, P < 0.05), while administration of MCT-induced PAH rats with MS-275 significantly reduced HDAC activity to 6.8 ± 0.15 RFU/μg (P < 0.05 versus MCT group), as presented in Fig. 4B. These findings indicate that inhibition of HDAC1 restores miR-34a expression through reducing deacetylation in MCT-induced PAH rats. The gene discussed is HDAC9; the disease is pulmonary arterial hypertension.