Role of 5-HT1A Receptor on Fluvoxamine induced Gastrointestinal Mucosa Protection and Healing in Animal with Stress-Induced Gastric Ulcer

Abstract

One factor that could contribute to the developing of gastric ulcer is stress. Fluvoxamine, an SSRI antidepressant showed protective effects to ulcers when administered before stress induction. In opposite, administration of fluvoxamine after stress induction delayed the mucosa healing. This study aimed to investigate the effects of pre-treatment and post-treatment of buspirone a 5-HT1A receptor partial agonist in the inhibition of gastric mucosal protection and healing by fluvoxamine in animals with stress-induced gastric ulcers. This study used ddY, male mice, weighed 25-30grams, which divided into two groups, pre-treatment and post-treatment groups. Each group consisted of subgroups that were administered low doses of buspirone (0.1mg/Kg and 0.3mg/Kg) and high doses of buspirone (10.0mg/Kg and 30.0mg/Kg). In the pre-treatment group, buspirone was administered intraperitoneally at 60 minutes before and continued with oral fluvoxamine 100mg/Kg administration at 30 minutes before stress induction. In the post-treatment group, buspirone was administered intraperitoneally followed fluvoxamine orally 30 minutes after stress induction done. The stress model used is water immersion restrain stress for 6 hours. In the pre-treatment group, the combination of high dose, but not low dose buspirone significantly inhibit the protection effects of fluvoxamine on stress-induced gastric ulcers. In addition, in the post-treatment group, the combination of low dose buspirone and fluvoxamine strengthen the delays of mucosal healing by fluvoxamine in mice with stress-induced gastric ulcers. Fluvoxamine protects and heals gastric mucosa from stress-induced gastric ulcer through the activation of 5HT1A receptor.