Application of an integrated loach-plant-substrate-microbes non-aerated saturated vertical flow constructed wetlands: Mechanisms of pollutants removal and greenhouse gases reduction.

This study established an integrated loach-plant-substrate-microbes non-aerated saturated vertical flow constructed wetlands (VFCWs) to enhance pollutants removal efficiencies and reduce greenhouse gas emissions simultaneously. The results of the VFCWs experiment indicated that the removal efficiencies of chemical oxygen demand, total phosphorous, and total nitrogen in loach systems were significantly higher than those of non-loach systems, achieving 59.16%, 35.98%, and 40.96%, respectively. The CH4 and N2O emission fluxes were also significantly reduced in the integrated system, resulting in lower global warming potential (GWP) and GWP per unit of pollutants removal. Loaches promoted the transportation of oxygen, facilitated the re-contact and utilization of sediments, reduced CH4 emission, and enhanced nitrogen conversion and phosphorus accumulation. Increased bioavailable carbon and nitrate-nitrogen in the integrated system improved the abundance of denitrifying bacteria, which supported complete denitrification, reducing N2O emissions with high pollutant removal.

Isorhynchophylline protects against pulmonary arterial hypertension and suppresses PASMCs proliferation.

Increased pulmonary arterial smooth muscle cells (PASMCs) proliferation is a key pathophysiological component of pulmonary vascular remodeling in pulmonary arterial hypertension (PAH). Isorhynchophylline (IRN) is a tetracyclic oxindole alkaloid isolated from the Chinese herbal medicine Uncaria rhynchophylla. It has long been used clinically for treatment of cardiovascular and cerebrovascular diseases. However, very little is known about whether IRN can influence the development of PAH. Here we examined the effect of IRN on monocrotaline (MCT) induced PAH in rats. Our data demonstrated that IRN prevented MCT induced PAH in rats, as assessed by right ventricular (RV) pressure, the weight ratio of RV to (left ventricular+septum) and RV hypertrophy. IRN significantly attenuated the percentage of fully muscularized small arterioles, the medial wall thickness, and the expression of smooth muscle α-actin (α-SMA) and proliferating cell nuclear antigen (PCNA). In vitro studies, IRN concentration-dependently inhibited the platelet-derived growth factor (PDGF)-BB-induced proliferation of PASMCs. Fluorescence-activated cell-sorting analysis showed that IRN caused G0/G1 phase cell cycle arrest. IRN-induced growth inhibition was associated with downregulation of Cyclin D1 and CDK6 as well as an increase in p27Kip1 levels in PDGF-BB-stimulated PASMCs. Moreover, IRN negatively modulated PDGF-BB-induced phosphorylation of PDGF-Rß, ERK1/2, Akt/GSK3ß, and signal transducers and activators of transcription 3 (STAT3). These results demonstrate that IRN could inhibit PASMCs proliferation and attenuate pulmonary vascular remodeling after MCT induction. These beneficial effects were at least through the inhibition of PDGF-Rß phosphorylation and its downstream signaling pathways. Therefore, IRN might be a potential candidate for the treatment of PAH.