Importance of gap junction in gastric mucosal restitution from acid-induced injury

Evidence is accumulating that gap junctional intercellular communication (G JIC) plays an important role in the gastric mucosal defense system. This st udy was conducted to determine whether GJIC mediates a restitution process in gastric mucosa. Male Sprague-Dawley rats were fasted and anesthetized. G astric injury was induced by luminal perfusion with 0.2N HCl for 10 minutes . Mucosal integrity wets continuously monitored by measuring the clearance of chromium 51-labeled ethylenediaminetetraacetic acid, which was used for analysis of recovery from the injury. Perfusion with 0.25% octanol (OCT; in hibitor of GJIC) was started after acid injury to assess its effect on rest itution. The effect of irsogladine (IG; activator of GJIC) was also tested, Gastric mucosal GJIC was immunohistochemically evaluated with monoclonal a ntibody gap junction protein (connexin 32). Recovery from acid-induced muco sal injury occurred rapidly when acid perfusion was discontinued (within ab out 60 minutes). OCT, which didn't cause any injury to normal gastric mucos a, significantly inhibited the restitution. IG reversed this inhibition in a dose-dependent manner. In an immunohistochemical study, OCT-induced damag e of gap junction was demonstrated, but not after IG pre-treatment. These f indings suggest that GJIC may play a critical role in restitution in rat ga stric mucosa and that gap junction function may be one of the important fac tors for the mucosal defense system.