Selenomethionine inhibits the proliferation of hypoxia-induced pulmonary artery smooth muscle cells by inhibiting ROS and HIF-1α-ACE-AngII axis.

Recent studies have shown that patients with pulmonary arterial hypertension (PAH) are deficient in nutrients, especially vitamins and minerals. Selenium is a strong antioxidant and there is a correlation between selenium and quality of life in patients with PAH. The purpose of this study was to research whether Selenomethionine (SeMet) can reduce the oxidative damage of pulmonary artery smooth muscle cells (PASMCs) and inhibit the proliferation of PASMCs in hypoxia, and the protective mechanism of SeMet on hypoxia-induced PASMCs. PASMCs were cultured and divided into 5 groups, normoxia group, hypoxia group, and hypoxia + SeMet group (10,20 and 40 µg/ml). It was found that cell activity was elevated and hyperproliferation was observed in the hypoxia group compared to the normoxia control group. Meanwhile, the antioxidant indexes SOD and CAT activities were reduced, T-AOC was decreased, and ROS and MDA contents were elevated in the hypoxia group. The expressions of HIF-1α, ACE, Ang II, VEGF genes and proteins in PASMCs were increased under hypoxia. And SeMet reversed the above changes in antioxidant indicators and proteins, thereby inhibiting the proliferation of PASMCs and promoting apoptosis. Our study found that SeMet may inhibit hypoxia-induced oxidative stress and proliferation in PASMCs by the ROS and HIF-1α-ACE-AngII axis.