الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
solubilizing effect of ethanol on gastric wall mucin. The gastric mucosal GSH level was significantly reduced whereas MDA was significantly elevated indicating an increase in ROS production.
Ethanol induced ulceration was also associated with a significant increase in inflammatory cytokines, TNF-α and IL-6 reflecting enhanced neutrophils infiltration into gastric mucosa. L-NAME pretreatment aggravated ethanol-induced ulceration together with an attenuation of the effect on mucin content of gastric juice and an augmentation of the alterations of the redox parameters. These effects could be related to the reduced GMBF as a result of diminished NO synthesis.
<Either systemic or central administration of ondansetron to control male rats produced a significant reduction in free and total acidity and peptic activity.
These effects could be mediated through blockade of central 5-HT3 receptors located either in vagal afferent neurons or in DMV with subsequent decrease in firing of the excitatory cholinergic pathway.
The reducing effect on peptic activity could also be mediated through the blockade of 5-HT3 receptors located in caudal raphe nuclei. On the other hand, the mucin content of the gastric juice was significantly increased by ondansetron treatment. This effect could be related to the inhibitory effect of ondansetron on HPA with subsequent elimination of the down-regulating effect of corticosteroids on MUC-1 gene expression and the biosynthesis of gastric mucin. Ondansetron treatment also significantly increased the mucosal content of GSH whereas MDA level was significantly reduced. These effects could be related to diminished corticosteroids that would reduce iNOS activity and the production of ROS. In addition, ondansetron may enhance NO release by inhibiting vagal activity and eliminating its downregulating effect on NO release from NANC division of vagal efferent neurons. NO is known to enhance GMBF and thus the disposal of ROS from tissues.
<Either systemic or central administration of ondansetron significantly attenuated indomethacin and ethanol-induced ulceration. The afforded protection ratio indicated a major contribution of central 5-HT3 receptors with a little contribution of the peripheral ones. In indomethacin-induced ulcer model, the protective effect of ondansetron was accompanied by a significant reduction of gastric acidity and peptic activity together with a significant increase in mucin content of gastric juice. Ondansetron pretreatment also significantly increased the mucosal content of GSH whereas MDA level was significantly reduced in both ulcer models. In addition, ondansetron lowered the mucosal content of inflammatory cytokines. Both L-NAME and glibenclamide abolished the gastroprotective effect conferred by ondansetron against both models of ulceration indicating that this gastroprotective effect is mediated through NO and KATP-dependent pathways. • Either systemic or central administration of aripiprazole to control rats produced a significant decrease in free and total acidity. This effect could be mediated through blockade of the facilitatory role of 5-HT2A receptors located on DVC and possibly on peripheral cholinergic neurons in gastric mucosa.