Tetrandrine prevents monocrotaline-induced pulmonary arterial hypertension in rats through regulation of the protein expression of inducible nitric oxide synthase and cyclic guanosine monophosphate-dependent protein kinase type 1

Pulmonary arterial hypertension (PAH) is a fatal cardiovascular disease. Proliferation of pulmonary artery smooth muscle cells, endothelial dysfunction, oxidative stress, and inflammation promote the development of pulmonary hypertension. Current therapies for PAH are limited, mostly designed to reduce pulmonary arterial resistance by inducing vasodilation. Tetrandrine, which was isolated from the root of Stephania tetrandra, was recognized to inhibit proliferation and to possess anti-inflammatory, antioxidant, antiallergic, and antifibrogenic activities. Whether tetrandrine has beneficial effects for the treatment of PAH is still unknown. The purpose of this study was to identify whether tetrandrine exerts beneficial effects on PAH and how it works.