Background Pulmonary arterial hypertension （PAH） is characterized by suppressing apoptosis and enhancing cell proliferation in the vascular wall. Inducing pulmonary artery smooth muscle cells （PASMC） apoptosis had been regarded as a therapeutic approach for PAH. Oridonin can cause apoptosis in many cell lines, while little has been done to evaluate its effect on PASMC. Methods Thirty male Sprague-Dawley rats were randomly assigned to three groups： normal control （NC）; hypoxia-hypercapnia （HH）; Hypoxia-hypercapnia ＋ oridonin （HHO）. Rats were exposed to hypoxia-hypercapnia for four weeks. Cultured human PASMC （HPASMC） were assigned to three groups： normoxia （NO）; hypoxia （HY）; hypoxia ＋ oridonin （HO）. The mean pulmonary artery pressure, mass ratio of right ventricle over left ventricle plus septum （RV/（LV＋S））, the ratio of thickness of the pulmonary arteriole wall to vascular external diameter （WT%） and the ratio of the vessel wall area to the total area （WA%） were measured. Morphologic changes of pulmonary arteries were observed under light and electron microscopes. The apoptotic characteristics in vitro and in vivo were detected. Results The mPAP, RW（LV＋S）, WT%, and WA% in the HH group were significantly greater than those in the NC （P 〈0.01） and HHO groups （P 〈0.01）; the activities of caspase-3 and caspase-9, and the expressions of Bax, cyt-C and apoptotic index （AI） in the group HH were less than those in the NC and HHO groups; and the expression of Bcl-2 in group HH was greater than that in the NC and HHO groups. HPASMC mitochondrial membrane potentials in group HO was lower than in group HY （P 〈0.01）, and cyt-C in the cytoplasm, AI, and caspase-9 in the HO group were greater than that in the HY group （P 〈0.01）, but the expression of Bcl-2 in the HO group was less than that in the HY group （P 〈0.05）. Conclusions The results suggest that oridonin can lower pulmonary artery pressure effectively, and inhibit pulm
WANG Liang-xingSUN YuCHEN ChanHUANG Xiao-yingLIN QuanQIAN Guo-qingDONG WeiCHEN Yan-fan
