학술논문

Rebamipide, an anti-ulcerative drug, inhibits induction of salivary dysfunction by benzodiazepines.
Document Type
Article
Source
Oral Diseases. May2017, Vol. 23 Issue 4, p511-517. 7p. 1 Diagram, 5 Graphs.
Subject
*SALIVA analysis
*BIOLOGICAL models
*COMBINATION drug therapy
*DIAZEPAM
*PAROTID glands
*RATS
*XEROSTOMIA
Language
ISSN
1354-523X
Abstract
Objectives The purpose of this study was to determine whether rebamipide, an antistomach ulcer agent, ameliorated benzodiazepine-induced hyposalivation in rat parotid gland ( PG) and submandibular gland ( SMG). Methods Saliva was collected from PG and SMG through a capillary cannula inserted into the parotid duct and sublingual papillae, respectively, every 15 min for 1 h after stimulation with pilocarpine dissolved in physiological saline and intraperitoneally administered at 1 mg kg−1. Diazepam ( DZP) was administered intraperitoneally at a dose of 0.2 mg kg−1 twice daily for 7 days. Rebamipide was administered at 10, 20, 30, or 100 mg kg−1 concomitantly with DZP to determine its effect on hyposalivation. The effect of rebamipide on movement of intracellular calcium ([Ca2+] i) in isolated parotid acinar cells was analyzed using Fluo4, a fluorescent dye used to detect Ca2+. Results Repetitive administration of DZP decreased salivary secretion in PG and SMG. This inhibitory effect was weakened by administration of rebamipide. Prior administration of DZP (10−6M) significantly suppressed carbachol (10−7M)-induced increase in [Ca2+] i. This inhibitory effect was ameliorated by combined use with rebamipide (5 × 10−4M). Conclusion This findings suggest that rebamipide weakens the downregulatory effect of DZP on salivary secretion by preventing DZP-induced suppression of increase in [Ca2+] i. [ABSTRACT FROM AUTHOR]