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[Formula: see text]mg/kg once two days) for 2 weeks after being injected with monocrotaline (MCT; 60[Formula: see text]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[Formula: see text]B was used to assess IL-1[Formula: see text], IL-6 and TNF-[Formula: see text] and WB was used to detect the total I[Formula: see text]B. Based on these measurements, it was found that APS reversed the MCT-induced increase in mean pulmonary arterial pressure (mPAP) (from 32.731[Formula: see text]mmHg to 26.707[Formula: see text]mmHg), decreased pulmonary vascular resistance (PVR) (from 289.021[Formula: see text]mmHg[Formula: see text][Formula: see text] min/L to 246.351[Formula: see text]mmHg[Formula: see text][Formula: see text][Formula: see text]min/L), and reduced right ventricular hypertrophy (from 289.021[Formula: see text]mmHg[Formula: see text][Formula: see text][Formula: see text]min/L to 246.351 mmHg[Formula: see text][Formula: see text][Formula: see text]min/L) ([Formula: see text]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[Formula: see text], IL-6 and TNF-[Formula: see text], reducing inflammation. Furthermore, APS was able to inhibit the activation of pho-I[Formula: see text]B[Formula: see text]. In couclusion, APS ameliorates MCT-induced pulmonary artery hypertension by inhibiting pulmonary arterial remodeling partially via eNOS/NO and NF-[Formula: see text]B signaling pathways.

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Background Gene fusion has epigenetic modification functions. The novel proteins encoded by gene fusion products play a role in cancer development. Therefore, a better understanding of the novel protein products may provide insights into the pathogenesis of tumors. However, the characteristics of chimeric genes are rarely studied. Here, we used weighted co-expression network analysis to investigate the biological roles and underlying mechanisms of chimeric genes. Methods Download the pig transcriptome data, we screened chimeric genes and parental genes from 688 sequences and 153 samples, predict their domains, and analyze their associations. We constructed a co-expression network of chimeric genes in pigs and conducted Gene Ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analysis on the generated modules using DAVID to identify key networks and modules related to chimeric genes. Results Our findings showed that most of the protein domains of chimeric genes were derived from fused pre-genes. Chimeric genes were enriched in modules involved in the negative regulation of cell proliferation and protein localization to centrosomes. In addition, the chimeric genes were related to the growth factor-β superfamily, which regulates cell growth and differentiation. Furthermore, in helper T cells, chimeric genes regulate the specific recognition of T cell receptors, implying that chimeric genes play a key role in the regulation pathway of T cells. Chimeric genes can produce new domains, and some chimeric genes are a key role involved in pathway-related function. Conclusions Most chimeric genes show binding activity. Domains of chimeric genes are derived from several combinations of parent genes. Chimeric genes play a key role in the regulation of several cellular pathways. Our findings may provide new directions to explore the roles of chimeric genes in tumors.

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