Capsiate is a non-pungent analogue of
capsaicin from CH-19 Sweet peppers.
Capsaicin is reported to trigger
calcitonin gene-related peptide (CGRP) release through activation of transient receptor potential vanilloid subfamily member 1 (TRPV1) and produces beneficial effects on gastric mucosa. This study aimed to investigate whether
capsiate is able to produce beneficial effects on gastric mucosa and whether the protective effects of capsipate occur through a mechanism involving the activation of TRPV1 and CGRP release. A rat model of gastric mucosal injury was established by the
oral administration of acidified
ethanol. Gastric tissues were collected for analysis of the
gastric ulcer index, cellular apoptosis, activities of
caspase-3,
catalase and
superoxide dismutase (SOD), and levels of CGRP, TNF-α, and
malondialdehyde (MDA). Our results show that the acute administration of
ethanol significantly increased the
gastric ulcer index concomitantly with an increase in cellular apoptosis,
caspase-3 activity, and TNF-α and MDA levels, as well as a decrease in the activities of
catalase and SOD. Pretreatment with 1 mg/kg
capsiate attenuated
ethanol-induced gastric mucosal injury and cellular apoptosis accompanied by an increase in CGRP level,
catalase, and SOD activities, and a decrease in
caspase-3 activity, and TNF-α and MDA levels. The effects of
capsiate were inhibited by
capsazepine, an antagonist of TRPV1. These results suggest that
capsiate is able to produce beneficial effects on
ethanol-induced gastric mucosal injury. These effects are related to the stimulation of CGRP release through the activation of TRPV1.