Astragalus Polysaccharides Attenuate Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats

Astragalus polysaccharides (APS) have been shown to possess a variety of biological activities including anti-oxidant and anti-inflammation functions in a number of diseases. However, their function in pulmonary arterial hypertension (PAH) is still unknown. Rats received APS (200 mg/kg once two days) for 2 weeks after being injected with monocrotaline (MCT; 60 mg/kg). The pulmonary hemodynamic index, right ventricular hypertrophy, and lung morphological features of the rat models were examined, as well as the NO/eNOS ratio of wet lung and dry lung weight and MPO. A qRT-PCR and p-I kappa B was used to assess IL-1 beta, IL-6 and TNF-alpha and WB was used to detect the total I kappa B. Based on these measurements, it was found that APS reversed the MCT-induced increase in mean pulmonary arterial pressure (mPAP) (from 32.731 mmHg to 26.707mmHg), decreased pulmonary vascular resistance (PVR) (from 289.021 mmHg x min/L to 246.351mmHg x min/L), and reduced right ventricular hypertrophy (from 289.021 mmHg x min/L to 246.351 mmHg x min/L) (p < 0.05). In terms of pulmonary artery remodeling, the WT% and WA% decreased with the addition of APS. In addition, it was found that APS promoted the synthesis of eNOS and the secretion of NO, promoting vasodilation and APS decreased the MCT-induced elevation of MPO, IL-1 beta, IL-6 and TNF-alpha, reducing inflammation. Furthermore, APS was able to inhibit the activation of pho-I kappa B alpha. In couclusion, APS ameliorates MCT-induced pulmonary artery hypertension by inhibiting pulmonary arterial remodeling partially via eNOS/NO and NF-kappa B signaling pathways.