AIMS: This study evaluated Na+,K+-ATPase activity and the abundance of alpha1 subunit Na+,K+-ATPase in experimental colitis and gathered evidence on the effects of interferon-gamma (IFN-gamma) on intestinal Na+,K+-ATPase. METHODS: Colitis was induced by the intrarectal administration of 2,4,6-trinitrobenzene sulphonic acid (TNBS, 30 mg/250 microL). Na+,K+-ATPase activity was determined as the difference between total and ouabain-insensitive ATPase. The abundance of Na+,K+-ATPase was analysed by immunoblotting. RESULTS: Na+,K+-ATPase activity was markedly reduced in the proximal colonic mucosa of TNBS-treated rats, whereas upstream in the terminal ileal mucosa a marked increase in sodium pump activity was observed. At the jejunal level no significant changes in Na+,K+-ATPase activity were observed between TNBS-treated rats and corresponding controls (ethanol-treated rats). No changes were observed in the abundance of alpha1 subunit Na+,K+-ATPase in the proximal colon, terminal ileum and jejunum. The administration of IFN-gamma (50,000 U) 48 h before sacrifice reduced both Na+,K+-ATPase activity and the abundance of alpha1 subunit Na+,K+-ATPase in the proximal colon. Dexamethasone prevented colonic inflammation and decreases in proximal colonic Na+,K+-ATPase activity in TNBS-treated rats, but did not affect the INF-gamma-induced decrease in colonic Na+,K+-ATPase activity. CONCLUSIONS: The increase in ileal Na+,K+-ATPase activity upstream to the lesioned colonic mucosa, where Na+,K+-ATPase activity was markedly reduced, might indicate a compensatory process to counteract the decrease in water and electrolyte absorption at the colonic level. This decrease in colonic Na+,K+-ATPase activity is likely not related to INF-gamma-induced downregulation of Na+,K+-ATPase.
AIMS: This study evaluated Na+,K+-ATPase activity and the abundance of alpha1 subunit Na+,K+-ATPase in experimental colitis and gathered evidence on the effects of interferon-gamma (IFN-gamma) on intestinal Na+,K+-ATPase. METHODS:Colitis was induced by the intrarectal administration of 2,4,6-trinitrobenzene sulphonic acid (TNBS, 30 mg/250 microL). Na+,K+-ATPase activity was determined as the difference between total and ouabain-insensitive ATPase. The abundance of Na+,K+-ATPase was analysed by immunoblotting. RESULTS: Na+,K+-ATPase activity was markedly reduced in the proximal colonic mucosa of TNBS-treated rats, whereas upstream in the terminal ileal mucosa a marked increase in sodium pump activity was observed. At the jejunal level no significant changes in Na+,K+-ATPase activity were observed between TNBS-treated rats and corresponding controls (ethanol-treated rats). No changes were observed in the abundance of alpha1 subunit Na+,K+-ATPase in the proximal colon, terminal ileum and jejunum. The administration of IFN-gamma (50,000 U) 48 h before sacrifice reduced both Na+,K+-ATPase activity and the abundance of alpha1 subunit Na+,K+-ATPase in the proximal colon. Dexamethasone prevented colonic inflammation and decreases in proximal colonic Na+,K+-ATPase activity in TNBS-treated rats, but did not affect the INF-gamma-induced decrease in colonic Na+,K+-ATPase activity. CONCLUSIONS: The increase in ileal Na+,K+-ATPase activity upstream to the lesioned colonic mucosa, where Na+,K+-ATPase activity was markedly reduced, might indicate a compensatory process to counteract the decrease in water and electrolyte absorption at the colonic level. This decrease in colonic Na+,K+-ATPase activity is likely not related to INF-gamma-induced downregulation of Na+,K+-ATPase.
Authors: María Laura Anzoise; Angeles Rodríguez Basso; Julieta Sofía Del Mauro; Andrea Carranza; Graciela López Ordieres; Susana Gorzalczany Journal: Inflammopharmacology Date: 2017-11-07 Impact factor: 4.473