Preventive Effect and Mechanism of Ethyl Acetate Extract of Sceptridium ternatum in Monocrotaline-Induced Pulmonary Arterial Hypertension.

Objective: To observe the effect and molecular mechanism of ethyl acetate extract of Sceptridium ternatum (STE) on the monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH).

Methods: The main chemical components of Sceptridium ternatum were determined, and the effects in PAH rats were observed. A total of 140 Sprague Dawley rats were randomly and equally divided into the normal group, the model group, the Bosentan group, and the STE groups (2.5, 5, 10 g/kg) by the random number table method. The characteristic indicators of PAH were measured, and immunohistochemistry was used to observe the lung tissue of rats. Morphological changes of the lung tissue were observed under the light microscope.

Results: Compared with the normal group, rats in the model group showed a significant increase in right ventricular free wall thickness (RVFWT), mean pulmonary arterial pressure (mPAP), mean right ventricular pressure (mRVP), max right ventricular pressure (max RVP), weight of right ventricle (RV), and lung index (LI), while a significant decrease in pulmonary artery acceleration time (PAAT, P<0.01). Compared with the model group, rats treated with STE had a significant decrease of RVFWT, mPAP, mRVP, max RVP, and RV, while a significant increase of PAAT (P<0.01). After injection of MCT, nuclear factor- κB (NF- κB) p65 and α -smooth muscle actin (α -SMA) expression levels were up-regulated, and on the contrary, the treatment groups showed a significant down-regulation without dose-dependent trend.

Conclusions: STE can relieve the PAH in rats. STE may relieve pulmonary vascular disease and pulmonary injury by down-regulating the expression of NF- κB p65 and α -SMA.