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Gastric juice and analysis of basal and stimulated secretion following treatment with rice-bran oil.

作者信息

Lloris J M, Bolant B, Gimeno L, Cejalvo D, Gimeno L O, Calvo M A, Perkins I

机构信息

Research Center, Valencia General and University Hospital, Spain.

出版信息

Res Commun Chem Pathol Pharmacol. 1991 Nov;74(2):245-8.

PMID:1811286
Abstract

In determining whether rice-bran oil (RBO) has antisecretory activity, we induced stress ulcers in 20 Wistar rats (10 controls; 10 animals given 0.2 ml/day RBO orally for 4 days prior to ulcer induction). In turn, we analyzed gastric juice for histamine, pepsin, H+ concentration ([H+]) and output volume. A second, complementary study was made of basal and stimulated gastric secretion through continuous "in vivo" recording of output. Secretion was stimulated with increasing doses of histamine, betanechol and pentagastrin. Ninety-four rats were used (47 controls and 47 rats given 0.2 ml/day RBO orally for 4 days prior to gastric output evaluation). The results were evaluated by the Student t-test. Ulcer index in the RBO-treated rats was significantly lower than among the controls (p less than 0.01), as also reflected by a significantly greater decrease in [H+] among the RBO-treated rats (p less than 0.05). However, no significant differences were observed for the remaining parameters. Continuous recording of basal gastric output showed a significant decrease in [H+] among the RBO-treated rats (p less than 0.01). Following histamine stimulation, [H+] was likewise significantly lower among the RBO-treated rats than in the controls. However, no significant differences were observed following stimulation with either betanechol or pentagastrin. RBO contains a high percentage of unsaturated fats; the latter act as precursors in the synthesis of arachidonic acid, which in turn is the essential precursor of prostaglandins--established inhibitors of gastric secretion. RBO also contains antioxidants such as alpha-tocopherol, which may likewise stimulate the synthesis of prostaglandins. RBO likely acts by increasing prostaglandin output, thus interfering with gastric HCl production.

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