Ribonuclease (RNase) reportedly exerts organ-protective effects in several pathological conditions, including ischemia reperfusion (I/R), but whether it can exhibit protective effect on intestinal I/R injury and potential mechanisms remain unknown. The present study was aimed to evaluate the effects of RNase on intestinal I/R injury and explore the underlying mechanisms. Thirty-two wild-type C57BL/6J adult male mice were evenly divided into a sham group, a sham + RNase group, an I/R group and an I/R + RNase group. Intestinal I/R was produced by clamping the superior mesenteric artery for 1 h followed by reperfusion for 2 h. All mice were treated with 3 doses of RNase or the same dosage of normal saline at different points. It was found that intestinal I/R caused significant intestinal injury and an increase in levels of extracellular RNAs (exRNAs). Treatment with RNase significantly reduced the inflammatory cytokine production, inhibited intestinal apoptosis and down-regulated the expression of toll like receptor 3 in intestinal tissues. In conclusion, increased exRNAs may contribute to intestinal I/R injury in adult mice, and RNase treatment during perioperative window is effective for attenuating intestinal I/R injury. V.Asthma, the most common chronic respiratory disease in the world, is involved in a sustained inflammatory response caused by a variety of immune cells. Ephedra with multi-target, multi-pathway functions is an effective treatment for asthma. However, the ingredients and anti-inflammatory targets of ephedra in treating asthma are unclear. Therefore, there is a need for further research. selleck Ephedra-related and anti-inflammatory targets were found and then combined to get intersection, which represented potential anti-inflammatory targets of ephedra. Moreover, compound-anti-inflammatory target and asthma-target protein-protein interaction network were merged to get the protein-protein interaction network intersection and core genes in asthma-target protein-protein interaction network. For the anti-inflammatory targets of ephedra in treating asthma, Gene Ontology and pathway analysis were executed to confirm gene functions of ephedra in antagonizing inflammation of asthma. Finally, molecular docking, qRT-PCR, WB and ELISA were performed to assess the binding activities between the compounds and anti-inflammatory targets of ephedra in treating asthma. Critical compounds and anti-inflammatory targets of ephedra in treating asthma were identified, including quercetin, luteolin, kempferol, naringenin, beta-sitosterol, SELE, IL-2 and CXCL10. The biological processes of anti-inflammatory targets of ephedra in treating asthma were involved in immune response, inflammatory response, cell-cell signaling and response to lipopolysaccharide. Moreover, 22 pathways were obtained and we proved that critical compounds inhabited the expression of SELE, IL-2 and CXCL10 at mRNA and protein levels. V.Prolactin-releasing peptide (PrRP) increases food intake in birds, whereas it is a potent satiety factor in rodents and fish. The aim of this study was to determine the effects of central injection of PrRP on feeding behaviors and hypothalamic physiology in juvenile Japanese quail (Coturnix japonica). Intracerebroventricular injection of 1,692 pmol of PrRP increased food intake for the first 90 min after injection but did not affect water intake. Quail treated with PrRP displayed more food and drink pecks, less time standing but more perching, and decreased defecations. Prolactin-releasing peptide-injected quail had increased c-Fos immunoreactivity in the dorsomedial nucleus (DMN) and arcuate nucleus (ARC) of the hypothalamus. Hypothalamic neuropeptide Y receptor subtypes 2 and 5 and melanocortin receptor 4 mRNAs were greater in PrRP- than vehicle-injected quail. In the DMN, there was less corticotropin-releasing factor (CRF) mRNA and in the ARC, more CRF mRNA in PrRP- than vehicle-injected chicks. Thus, PrRP increases food intake in quail, which is associated with changes in hypothalamic CRF and neuropeptide Y receptor gene expression and c-Fos-immunolabeled cells in the ARC and DMN. Zymosan is a cell wall component of the yeast Saccharomyces cerevisiae and produces severe inflammatory responses in mammals. When zymosan is peripherally injected in mammals, it induces several behavioral and physiological changes including anorexia and hyperthermia. However, to our knowledge, behavioral and physiological responses to zymosan have not yet been clarified in birds. Therefore, the purpose of the present study was to determine if intraperitoneal injection of zymosan affects food intake, voluntary activity, cloacal temperature, plasma corticosterone (CORT) and glucose concentrations, and splenic gene expression of cytokines in chicks (Gallus gallus). Intraperitoneal injection of zymosan (2.5 mg) significantly decreased food intake, voluntary activity, and plasma glucose concentration, and increased plasma CORT concentration. The injection of 0.5 mg zymosan significantly increased cloacal temperature, while 2.5 mg zymosan had a tendency to increase it. Finally, 2.5 mg zymosan significantly increased the splenic gene expression of interleukin-1β (IL-1β), IL-6, IL-8, interferon-γ, and tumor necrosis factor-like cytokine 1A. The present results suggest that zymosan would be one of components which induces nonspecific symptoms including anorexia, hypoactivity, hyperthermia, and stress responses, under fungus infection in chicks. Friedreich ataxia (FA) is a cardioneurodegenerative disease caused by deficient frataxin expression. This mitochondrial protein has been related to iron homeostasis, energy metabolism, and oxidative stress. Previously, we set up a cardiac cellular model of FA based on neonatal rat cardiac myocytes (NRVM) and lentivirus-mediated frataxin RNA interference. These frataxin-deficient NRVMs presented lipid droplet accumulation, mitochondrial swelling and signs of oxidative stress. Therefore, we decided to explore the presence of protein thiol modifications in this model. With this purpose, reduced glutathione (GSH) levels were measured and the presence of glutathionylated proteins was analyzed. We observed decreased GSH content and increased presence of glutahionylated actin in frataxin-deficient NRVMs. Moreover, the presence of oxidized cysteine residues was investigated using the thiol-reactive fluorescent probe iodoacetamide-Bodipy and 2D-gel electrophoresis. With this approach, we identified two proteins with altered redox status in frataxin-deficient NRVMs electron transfer flavoprotein-ubiquinone oxidoreductase and dihydrolipoyl dehydrogenase (DLDH).