linoleic-acid and Stomach-Ulcer

Gastric ulcer has been a major cause of morbidity and mortality worldwide, and it has been linked to factors such as nutritional deficiency, smoking, stress, and continuous intake of non-steroidal antiinflammatory drugs (NSAIDs). The search for new anti-ulcer therapeutic agents has been the subject of several studies. Recently, the gastroprotective effect of Celtis iguanaea has been reported, with linoleic acid (LA) responsible for many of the therapeutic effects of this medicinal plant.. This study aims to investigate the gastroprotective activity and the possible mechanisms in which LA may be involved through different experimental assays in mice.. The gastroprotective activity of LA was evaluated in the ulcer induced by indomethacin, HCl/EtOH, hypothermic-restraint stress and pyloric ligation. For the investigation of gastroprotective mechanisms, the quantification of the volume (mL), pH and total acidity of gastric secretion were considered.. The oral administrations of 25 mg/kg, 50 mg/kg or 100 mg/kg of body weight of LA were capable of protecting the gastric mucosa against HCl/ethanol (10 mL/kg p.o.), and oral/intraduodenal treatment administrations of 50 mg/kg LA showed protection from ulcers induced by indomethacin, hypothermic-restraint stress and pyloric ligation.. The results of this study show the gastroprotective role of LA in gastric mucosal damage induced by all assayed distresses. The observed gastroprotection possibly occurs due to the mediated increase of mucosal defensive factors.

Topics: Animals; Anti-Ulcer Agents; Disease Models, Animal; Ethanol; Gastric Mucosa; Humans; Indomethacin; Linoleic Acid; Mice; Plant Extracts; Stomach Ulcer

The Opuntia ficus indica f. inermis methanolic flowers extract (OMFE) was phytochemical studied, in vitro tested for their potential antioxidant activity using 2,2-diphenyl-1-picrylhydrazyl (DPPH), reducing power, linoleic acid peroxidation assays and in vivo evaluated for its ability to prevent ethanol-induced gastric ulcer in rats. The OMFE was rich in polysaccharide, phenolics and flavonoids contents and exhibited a moderate in vitro antioxidant activity when compared with (+)-catechin and ascorbic acid. Pre-treatment with OMFE at oral doses 250, 500 and 1000 mg/kg body weight was found to provide a dose-dependent protection against ethanol-induced gastric ulcer by averting the deep necrotic lesions of the gastric epithelium, by preserving normal antioxidant enzymes activities, by inhibiting the lipid peroxidation, the oxidation of protein and the DNA fragmentation in gastric mucosa. The antiulcerogenic activity of OMFE might be due to a possible synergistic antioxidant and antihistaminic-like effects.

Topics: Animals; Anti-Ulcer Agents; Antioxidants; DNA Fragmentation; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; Enzymes; Ethanol; Flavonoids; Flowers; Free Radical Scavengers; Intestinal Mucosa; Linoleic Acid; Lipid Peroxidation; Male; Opuntia; Phenols; Plant Extracts; Rats; Rats, Wistar; Stomach Ulcer; Toxicity Tests, Acute

This study investigated the effects of Onosma armeniacum K. (Boraginaceae) root extract (AR-1) on ethanol-induced stomach ulcers, and on some oxidant and antioxidant parameters, in stomach tissue in rats. The results obtained showed that AR-1 significantly inhibited ethanol-induced ulcers at 25, 50, 100 and 200 mg/kg doses. We found that 50, 100 and 200 mg/kg doses of AR-1 inhibited ulcers more effectively than did ranitidine. AR-1 at doses of 25, 50, 100 and 200 mg/kg significantly prevented the decrease in total glutathione (tGSH) level which occurs in damaged stomach tissues of rats given ethanol (control group). Only a 100 mg/kg dose of AR-1 significantly increased the glutathione S-transferase (GST) level in stomach tissue compared to the control. All doses of AR-1 except the 25 mg/kg dose eliminated the decrease in the superoxide dismutase (SOD) level in the stomach tissue of rats given ethanol. While all doses of AR-1 decreased malondialdehyde (MDA) levels significantly; all doses AR-1 except 25 mg/kg decreased myeloperoxidase (MPO) levels significantly compared to the control. The effect of AR-1 on catalase (CAT) activity was insignificant at all doses. AR-1 significantly increased nitric oxide (NO) levels at 50, 100 and 200 mg/kg doses compared to the control. Our results indicate that the protection of some antioxidant mechanisms and the inhibition of some oxidant mechanisms have a role in AR-1's antiulcer effect mechanism.

Topics: Animals; Boraginaceae; Catalase; Ethanol; Gastric Mucosa; Glutathione; Glutathione Transferase; Linoleic Acid; Lipid Peroxidation; Malondialdehyde; Nitric Oxide; Oxidative Stress; Peroxidase; Phytotherapy; Plant Extracts; Plant Roots; Ranitidine; Rats; Rats, Wistar; Stomach; Stomach Ulcer; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances

Rats were fed diets containing different ratios of linoleate (18:2 n-6) to alpha-linolenate (18:3 n-3), and the severity of gastric injury induced by ethanol, ischemia/reperfusion and water-immersion stress was compared. On decreasing the 18:2 n-6/18:3 n-3 ratios in the diets, the proportion of arachidonic acid (20:4 n-6) decreased and that of eicosapentaenoic acid (20:5 n-3) increased in the phospholipids of the gastric mucosa, which was associated with decreased mucosal prostaglandin E2 content. Mucosal injury in all the three experimental models was exacerbated significantly in the diet group fed 18:2 n-6/18:3 n-3 ratio of 0.25 (perilla oil) as compared with the groups fed dietary oils with 18:2 n-6/18:3 n-3 ratios of 2.7 (mixture of perilla and safflower oils) and 127 (safflower oil). This adverse effect induced by perilla oil diet was not observed when rats were pretreated with a mild irritant (20% ethanol) prior to challenge with a strong irritant (absolute ethanol). Furthermore, an 18:2 n-6/18:3 n-3 ratio of as low as 1 was found to be in a safe range in the water-immersion stress ulcer model. Thus, oils with very low n-6/n-3 ratios, for example perilla oil, could be used without the risk of the observed adverse effects on experimental gastric injury in people of industrialized countries ingesting foods with n-6/n-3 ratios of above 4. A decrease in the n-6/n-3 ratios to 2 or below is still recommended for the prevention of chronic diseases in the elderly related to atherosclerosis and inflammation.

Topics: alpha-Linolenic Acid; Animals; Diet; Dietary Fats, Unsaturated; Dinoprostone; Disease Models, Animal; Ethanol; Fatty Acids; Gastric Acid; Gastric Mucosa; Linoleic Acid; Male; Pepsin A; Phospholipids; Plant Oils; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Stomach Ulcer

We studied chronic intake of diets deficient in or supplemented with linoleic acid to determine whether it affects gastric acid secretion, release of prostaglandin E2, and stress-induced lesions. For 8-10 wk rats were fed three dietary regimens supplying 3.5% (control group), 0.3%, and 10% of total calories as linoleic acid. We found that diets deficient in linoleic acid (0.3%) reduced release of prostaglandin E2 into the gastric lumen (-77%) and increased basal (+133%) and pentagastrin-stimulated acid secretion (+93%) and the area of cold restraint-induced gastric mucosal lesions (+280%), when compared with the control group. Diets supplemented with linoleic acid (10%) increased prostaglandin E2 release into the gastric lumen (+106%) and reduced basal (-44%) and pentagastrin-stimulated acid secretion (-78%) and the area of cold restraint-induced mucosal.lesions (-80%). Prevention of these lesions by the 10% linoleic acid diet was confirmed by quantitative histology. Pretreatment with indomethacin (8 mg/kg intraperitoneally) abolished the effects of the 10% linoleic acid diet on prostaglandin formation, acid secretion, and mucosal injury. We conclude that in rats chronic intake of dietary linoleic acid reduces acid secretion and prevents cold restraint-induced mucosal lesions, possibly because of augmented synthesis of endogenous prostaglandins in the gastric mucosa.

Topics: Animals; Diet; Dinoprostone; Female; Fistula; Gastric Juice; Gastric Mucosa; Indomethacin; Ligation; Linoleic Acid; Linoleic Acids; Pentagastrin; Prostaglandins E; Pylorus; Rats; Rats, Inbred Strains; Stomach Ulcer; Stress, Physiological