Search in the Abstract Database

Search Abstracts 2013

* = Presenting author

P015. The influence of COX-1/COX-2 inhibitors on the Na/Li-countertransport and Na,K,2Cl-cotransport in erythrocytes of rats with experimental colitis

N. Grynchyshyn1, 1Danylo Halytsky Lviv National Medical University, Ukraine


Ulcerative colitis is a chronic inflammatory disease, accompanied by acute increase of lipoperoxidation processes, causing the damage of cell membrane and ion exchange disorders. It is known, that the inflammatory process are characterized by increased expression of COX-1/COX-2 isoforms. The aim of present study was to investigate the activity of Na/Li-countertransport and Na,K,2Cl-cotransport in erythrocytes of rats with experimental colitis and to determine their succeptibility to the influence of COX-1/COX-2 and selective COX-2 blockage.


40 male rats were divided into 4 groups: 1st – control rats (n = 10); 2nd – rats with acetic acid-induced colitis (n = 10); 3rd (n = 10) and 4th (n = 10) groups included the rats, exposed to the effect of COX-1/COX-2 inhibitor indomethacin and selective COX-2 inhibitor celecoxib dosed 10 mg/kg b.w. twice – before the induction of colitis and a day after. The activity of Na/Li-countertransport as a membrane function, which exchanges intracellular Na for extracellular Li and Na,K,2Cl cotransport in erythrocytes of rats were assessed, using standard pharmacokinetic methodics (Canessa M., 1989).


The increase of the standard Na/Li countertransport activity was revealed in rats with experimental colitis (3.86±0.26 mmol Na+ × L cells(−1) × h(−1) vs. 2.98±0.39 mmol Na+ × L cells(−1) × h(−1) in control group, P < 0.05). The nonsignificant decrease of Na,K,2Cl-cotransport activity was observed between measurements obtained in control group and in acetic acid-induced colitis (8.56±0.71 mmol Na+ × L cells(−1) × h(−1) vs. 7.92±0.58 mmol Na+ × L cells(−1) × h(−1) accordingly). The effect of indomethacin caused depression of velocity of Na/Li-countertransport in erythrocytes of rats with experimental colitis but it induced ulcerative lesions of the gastrointestinal tract. The effect of celecoxib caused normalization of Na-transporting function of erythrocytes and cell ion homeostasis.


Experimental colitis caused increased permeability of erythrocyte membrane for the ions and changes of quabaininsensitive Na-transport mechanisms. Selective COX-2 inhibition by celecoxib showed effective anti-inflammatory effect and corrected the disorders of Na-transporting systems as well as decreased the level of oxidative stress in blood.