Mucosal protective effects of ecabet sodium: pepsin inhibition and interaction with mucus

Abstract

Pepsin, acid and Helicobacter pylori are major factors in the pathophysiology of peptic ulcer disease and reflux oesophagitis. Ecabet sodium reduces the survival of H. pylori in the stomach and inhibits pepsin activity in the gastric juice of experimental animals. Here we have investigated the effects of ecabet sodium on some of the factors involved in the dynamics of the mucosal barrier, i.e. pepsins and mucins. This study used gastric juice obtained from 12 non-symptomatic volunteers and nine patients with reflux oesophagitis. Ecabet sodium significantly inhibited pepsin activity in human gastric juice, with a maximum inhibition of 78%. Pepsin 1, the ulcer-associated pepsin, was inhibited to the greatest extent. The ability of gastric juice to digest mucin was significantly inhibited by ecabet. As with gastric juice proteolytic activity, the inhibitory effect of ecabet on mucolysis was greater in gastric juice from patients with reflux oesophagitis than in that from controls. Ecabet sodium showed a positive interaction with gastric mucin, as assessed by an increase in viscosity. Thus ecabet sodium may reduce the aggressive potential of gastric juice towards the mucosa, which may be relevant in the treatment of reflux oesophagitis and peptic ulcer disease. In addition, it may strengthen the mucus barrier in peptic ulcer disease and gastritis.

Gastroprotective activity of ferruginol in mice and rats: effects on gastric secretion, endogenous prostaglandins and non-protein sulfhydryls

“…The study of the mechanism underlying this protective effect has pointed out that many of these compounds act by reinforcing the defensive factors in the gastric mucosa such as stimulation of prostaglandin synthesis, increase of mucus production or improvement of the mucosal antioxidant capacity (Onoda et al 1990;Wada et al 1997;Ichikawa et al 2000;Rodríguez et al 2005). On the other hand, some of these gastroprotective diterpenes seem to reduce the activity of the aggressive factors in the stomach such as pepsin or acid secretion (Pearson & Roberts 2001;Hiruma-Lima et al 2002).…”

Characteristic pathological findings and effects of ecabet sodium in rat reflux esophagitis

“…ES, a dehydroabietic acid derivative from pine resin, has been used clinically in the treatment of gastritis and gastric ulcer, and is believed to exert its effects through various mechanisms [20][21][22][23][24] . ES binds directly to the gastric mucosa, thereby protecting the mucosa against ethanol binding, and it has been shown to inhibit pepsin activity in rat and human gastric juices.…”

Ecabet sodium inhibitsHelicobacter pylorilipopolysaccharide-induced activation of NADPH oxidase 1 or apoptosis of guinea pig gastric mucosal cells

“…This agent has a high affinity for gastric mucus and is known to inhibit pepsin (29) and urease activities (15). Ecabet is also suggested to improve efficacy of antibiotic therapy for H. pylori infection in patients with peptic ulcer (1,16).…”