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Showing 3 results for Gharibnaseri

Mohammad Kazem Gharibnaseri, Seyed Ali Mard,
Volume 10, Issue 4 (Winter 2007)
Abstract

Introduction: Alhagi camelorum belongs to the Leguminosae family is used in Iranian folk medicine to treat some gastric diseases. The present study was undertaken to evaluate the Alhagi camelorum aqueous extract for anti-ulcer activity in rats. Methods: Male Wistar rats were pretreated with the A. camelorum aqueous extract (150, 300 or 450 mg/kg of B.W., P.O.) before induction of gastric ulcer by water immersion restraint-stress at 20-22 °C (5 h) or before induction of the ulcer by ethanol 100% (1 ml/200g of B.W., P.O.). Negative control animals received saline (0.5 ml/100 g of B.W.). Positive control animals received ranitidine (60 mg/kg, P.O.). Results: The A. camelorum aqueous extract (ACE) protected rats against water immersion restraint-stress and ethanol-induced ulcers in a dose-dependent manner. In water immersion restraint induced ulcerated rat, the ACE increased pH and reduced gastric acid content. ACE did not show any signs of toxicity and mortality up to10 g/kg, P.O. in mice. Conclusion: The results suggest that A. camelorum aqueous extract can exert significant mucosal protection and antisecretory effects on gastric mucosa in rats.
Mohammadkazem Gharibnaseri, Leila Zarepoor, Samad Mojab,
Volume 11, Issue 1 (Spring 2007)
Abstract

Introduction: Mental stress is one of the most important causes of the gastric ulcer. On the other hand, flavonoids such as quercetin show protective effects. The aim of this study was to investigate possible protective effect of quercetin on water restraint stress-induced ulcer in rats. Methods: Adult male Wistar rats were divided into seven groups each containing eight animals. The first group (S) received normal saline (5 ml/kg, p.o.) and groups 2-7 received normal saline, quercetin 25, 50, 100, 200 (mg/kg, p.o.) or omeprazole (20 mg/kg, s.c.) respectively. After 1 hour, all animals except the first group (S) were placed into the plexiglass restrainers and kept in water (23°C) for 3.5 hours. After another 3.5 hours interval, rats were scarified and volume of gastric output, pH, acid content and ulcer index (UI) were measured. Results: pH of gastric content in QS50-QS200 groups was lower than the saline/stress (SS) treated group (P<0.05). The gastric acid content in the saline treated group was higher than SS, quercetin/stress (QS) 50 and QS 200 groups (P<0.05) and higher than omeprazole/saline (OS) group. Omeprazole inhibited the gastric acid secretion. The UI in the QS25 and QS50 groups were lower than of SS group (P<0.05 and P<0.01 respectively) The UI in the QS100 and QS200 groups were identical to SS group. The UI in S and OS groups was approximately zero. Conclusion: The results of this study suggest the protective effect of quercetin in stress-induced gastric ulcer test. However this protective effect is not precisely dose independent.
Seyyed Ali Mard, Mohamad Kazem Gharibnaseri,
Volume 11, Issue 1 (Spring 2007)
Abstract

Introduction: The effect of esophageal distension (ED) on gastric motility has been well documented, but a few investigations have been carried out on the effect of ED on gastric secretion. The aim of this study was to investigate the effect of ED on gastric acid and pepsin secretion and the mechanism(s) involved. Methods: Male adult Wistar rats (200-240 g) were anesthetized with urethane (1.2 g/kg, i.p.) and underwent tracheostomy and laparotomy. A catheter was inserted in the stomach through duodenum for gastric distension and gastric washout. Esophagus was distended by a balloon (0.3 ml, 10 min). Gastric acid secretion was stimulated by gastric distension (by saline 1.5 ml/100 g of B.W.), pentagastrin (20 μg/kg, i.p.) or insulin (0.6 IU/kg, i.p.). Pepsin secretion was stimulated by carbachol (20 μg/kg, i.p.). Effects of cervical vagotomy and reserpine (1 mg/kg, i.p.) were also investigated. Results: Gastric distension-, pentagastrin- and insulin-stimulated gastric acid secretion were decreased by esophageal distension (P<0.001, P<0.05 and P<0.05, respectively). Carbachol-induced pepsin secretion was also attenuated by esophageal distension (P<0.05). Cervical vagotomy abolished the inhibitory effect of ED on gastric distension-induced acid secretion. In reserpinized rats, ED reduced the basal gastric acid secretion (P<0.05). Conclusion: Results indicated that the ED decreased gastric acid output. The vagus nerve was involved in the inhibitory effect of the ED on gastric acid secretion but the adrenergic system did not play role.

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