Pretreatment with water kefir reduces the development of acidified ethanol-induced gastric ulcers

Abstract

To evaluate the gastroprotective and antioxidant effects of pretreatment with water kefir on ulcers induced with HCl/ethanol. All pretreatments lasted 14 days. Male mice were separated into five groups: the control (C) group received vehicle without ulcer induction; the ulcerated (U) group received vehicle; the lansoprazole (L) group received 30 mg/kg/day lansoprazole; the water kefir (WK15 and WK30) groups received WK at a dose of 0.15 or 0.30 ml/kg/day, respectively. Gastroprotection was measured by ulcer area, ulcer index and ulcer reduction percentage. Antioxidant effects were quantified by measuring advanced oxidized protein products (AOPPs), superoxide dismutase (SOD), and catalase activity in the stomach. Pretreatment with WK at both doses promoted gastroprotection against HCl/ethanol-induced ulcers much like the pretreatment with lansoprazole. In addition, WK decreased protein oxidation while increasing SOD and catalase activity. We concluded that pretreatment with water kefir increases the activity of antioxidant enzymes, preventing gastric lesions induced by HCl/ethanol by maintaining the antioxidant performance in gastric tissue.

Pathological and histomorphometric study of comparative gastric ulcer induced by indomethacin, aspirin, and ethanol in rats

“…The gross appearance of rats' stomachs of the indomethacin and ethanol groups revealed severe mucosa redness after 3 hrs of ulcer induction with the site of erosions or gastric ulcers were obvious and more in number in the ethanol group. The gastric ulcers were more evident and had high numbers in all three groups after 24 hrs of gastric ulcer induction, which agrees and corresponds with the many studies that animal studies frequently use the ethanol and Indomethacin-induced gastric ulcer model (3,(25)(26)(27). The administration of ethanol reduces the release of bicarbonate, nitric oxide, and gastric mucus, with subsequent necrosis and damage of gastric mucosa and infiltration of inflammatory cells.…”

“…Gastric ulceration is a necrotizing mucosa lesion leading to inflammation and hemorrhage because of damage and perforation of the gastric mucosa (1). When the stomach is exposed to excessive acid and intense pepsin activity, gastrointestinal toxicity of non-steroidal anti-inflammatory drugs (NSAIDs), and toxic substances like alcohol use, it is the most common gastrointestinal disorder ever reported (2,3). Gastric ulcers occur due to the difference between potentially destructive and defensive factors of the gastric mucosa (4).…”