AIM: To study the effect of hypoxia and hypercapnia on nitric oxide (NO) in plasma and superoxide dismutase (SOD), catalase (CAT), soluble guanylate cyclase (sGC), cyclic guanosine monophospholate (cGMP) in lung tissue in rats, and to explore the effect of NO- and H_2O_2-sGC pathway on the development of the pulmonary hypertension. METHODS: The model of hypoxic and hypercapnic 1, 2, 4-week group (HH 1 week, HH 2 weeks, HH 4 weeks) and control group was set up. NO content in plasma, CAT and SOD in rat lung were determined by spectrophotometry. The sGC activity in lung tissue was detected by enzyme kinetic analysis. cGMP content in lung tissue was examined with ~ 125 I-radioimmunoassay. RESULTS: The mean pulmonary artery pressure (mPAP) showed significantly higher in HH 1 week, HH 2 weeks and HH 4 weeks groups compared with control group (all P

Objective To investigate the expression of IFN-γ, IL-5, IL-17 and TGF-βby Th cells and Th17 cells in rats with allergic rhinitis upon the intervention of IL-10.Methods SD rats were ran-domly divided into three groups including allergic rhinitis ( AR ) group, IL-10 treated group and control group (n=10).Rats in AR group and IL-10 treated group were sensitized by injection of ovalbumin (OVA) and aluminum hydroxide on the 1st, the 7th and the 14th days.The rats treated with equal volume of saline were set up as the control.The corresponding interventions ( OVA, OVA and IL-10, saline) were respec-tively given to rats in each group on the 21th day for 7 consecutive days.The clinical manifestations in rats were observed within 30 minutes after each administration.Serum samples were collected at 48 hours after the last challenge for the detection of IgE and OVA-sIgE.ELISA and Western blot assay were performed to detect IFN-γ, IL-5, IL-17 and TGF-βin nasal mucosa samples.Results Some characteristic symptoms of AR were observed in rats from AR group and IL-10 treated group.Compared with IL-10 treated rats, rats in AR group showed severe clinical symptoms such as constant rubbing and tearing of the eyes (P<0.05).The levels of IgE and OVA-sIgE in serum samples and the levels of IFN-γ, IL-5, IL-17 and TGF-βin nasal tis-sues were significantly increased in rats with RA (P<0.05), but were reduced with IL-10 intervention (P<0.05).Conclusion Exogenous IL-10 could be used to treat AR by reducing the expression of IFN-γ, IL-5, IL-17 and TGF-βin nasal tissues.

OBJECTIVE: To investigate the expression of galectin-1 with the stimulation of peritoneal dialysis solution (PDS) and its role in the epithelial-to-mesenchymal transition (EMT) in human peritoneal mesothelial cells (HPMCs). METHODS: HPMCs were stimulated with PDS containing different concentrations of high glucose (1.5%, 2.5%, and 4.25%). After 24 h, mRNA and protein expressions of galectin-1,vimentin, and zo-1 were analyzed with real-time PCR and Western blot, respectively. Liposome transfected siRNA technique was used to knock down the expression of galectin-1 and the effect of galectin-1 siRNA on the EMT of HPMCs was also observed under 4.25% PDS condition. RESULTS: mRNA expression of galectin-1 in HPMCs increased in PDS groups, especially in group with 4.25% PDS (P<0.05). Protein expression of galectin-1 in HPMCs significantly increased in PDS groups with a dose dependent manner (P<0.05).Expression of vimentin in HPMCs significantly increased in PDS groups, especially in groups of 2.5% PDS and 4.25% PDS (P<0.05), but zo-1 expression markedly decreased (P<0.05). The expression of galectin-1 correlated positively with vimentin (P<0.05) but negatively with zo-1 (P<0.05). Expression of vimentin in groups of 4.25% PDS was markedly inhibited (P<0.05) by galectin-1 siRNA, whereas zo-1 expression was significantly increased (P<0.05). CONCLUSION Galectin-1 can mediate high glucose PDS-induced EMT in HPMCs and may be a new target for the prevention and treatment of peritoneal fibrosis.
Cells, Cultured ; Dialysis Solutions ; pharmacology ; Epithelial Cells ; cytology ; Epithelial-Mesenchymal Transition ; drug effects ; Galectin 1 ; genetics ; metabolism ; Glucose ; pharmacology ; Humans ; Peritoneal Dialysis ; adverse effects ; Peritoneal Fibrosis ; etiology ; Peritoneum ; cytology ; RNA, Messenger ; genetics ; metabolism