title: Beneficial effects of capsiate on ethanol-induced mucosal injury in rats are related to stimulation of calcitonin gene-related Peptide release.
abstract: 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.
authors.affiliation: Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, China.
authors.forename: Nian-Sheng
authors.initials: NS
authors.lastname: Li
authors.forename: Xiu-Ju
authors.initials: XJ
authors.lastname: Luo
authors.forename: Zhong
authors.initials: Z
authors.lastname: Dai
authors.forename: Bin
authors.initials: B
authors.lastname: Liu
authors.forename: Yi-Shuai
authors.initials: YS
authors.lastname: Zhang
authors.forename: Zhi-Chun
authors.initials: ZC
authors.lastname: Yang
authors.forename: Jun
authors.initials: J
authors.lastname: Peng
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism*; D002211:Capsaicin / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D002212:Capsicum / Q000737:chemistry*; D053148:Caspase 3 / Q000378:metabolism; D004195:Disease Models, Animal; D000431:Ethanol; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism; D005765:Gastrointestinal Agents / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D013276:Stomach Ulcer / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D050916:TRPV Cation Channels / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D005765:Gastrointestinal Agents; D010936:Plant Extracts; D050916:TRPV Cation Channels; C494484:TRPV1 receptor; D014409:Tumor Necrosis Factor-alpha; D000431:Ethanol; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D053148:Caspase 3; D015740:Calcitonin Gene-Related Peptide; C470213:capsiate; D002211:Capsaicin