PT  - JOURNAL ARTICLE
AU  - Jand Venes R. Medeiros
AU  - Víctor H. Bezerra
AU  - Antoniella S. Gomes
AU  - André Luiz R. Barbosa
AU  - Roberto César P. Lima-Júnior
AU  - Pedro Marcos G. Soares
AU  - Gerly Anne C. Brito
AU  - Ronaldo A. Ribeiro
AU  - Fernando Q. Cunha
AU  - Marcellus H. L. P. Souza
TI  - Hydrogen Sulfide Prevents Ethanol-Induced Gastric Damage in Mice: Role of ATP-Sensitive Potassium Channels and Capsaicin-Sensitive Primary Afferent Neurons
AID  - 10.1124/jpet.109.152801
DP  - 2009 Sep 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 764--770
VI  - 330
IP  - 3
4099  - http://jpet.aspetjournals.org/content/330/3/764.short
4100  - http://jpet.aspetjournals.org/content/330/3/764.full
SO  - J Pharmacol Exp Ther2009 Sep 01; 330
AB  - The aim of this study was to evaluate the protective effect of hydrogen sulfide (H2S) on ethanol-induced gastric lesions in mice and the influence of ATP-sensitive potassium (KATP) channels, capsaicin-sensitive sensory afferent neurons, and transient receptor potential vanilloid (TRPV) 1 receptors on such an effect. Saline and l-cysteine alone or with propargylglycine, sodium hydrogen sulfide (NaHS), or Lawesson's reagent were administrated for testing purposes. For other experiments, mice were pretreated with glibenclamide, neurotoxic doses of capsaicin, or capsazepine. Afterward, mice received l-cysteine, NaHS, or Lawesson's reagent. After 30 min, 50% ethanol was administrated by gavage. After 1 h, mice were sacrificed, and gastric damage was evaluated by macroscopic and microscopic analyses. l-Cysteine, NaHS, and Lawesson's reagent treatment prevented ethanol-induced macroscopic and microscopic gastric damage in a dose-dependent manner. Administration of propargylglycine, an inhibitor of endogenous H2S synthesis, reversed gastric protection induced by l-cysteine. Glibenclamide reversed l-cysteine, NaHS, or Lawesson's reagent gastroprotective effects against ethanol-induced macroscopic damage in a dose-dependent manner. Chemical ablation of sensory afferent neurons by capsaicin reversed gastroprotective effects of l-cysteine or H2S donors (NaHS or Lawesson's reagent) in ethanol-induced macroscopic gastric damage. Likewise, in the presence of the TRPV1 antagonist capsazepine, the gastroprotective effects of l-cysteine, NaHS, or Lawesson's reagent were also abolished. Our results suggest that H2S prevents ethanol-induced gastric damage. Although there are many mechanisms through which this effect can occur, our data support the hypothesis that the activation of KATP channels and afferent neurons/TRPV1 receptors is of primary importance. The American Society for Pharmacology and Experimental Therapeutics