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Hydrogen Sulfide Prevents Ethanol-Induced Gastric Damage in Mice: Role of ATP-Sensitive Potassium Channels and Capsaicin-Sensitive Primary Afferent Neurons

2009; American Society for Pharmacology and Experimental Therapeutics; Volume: 330; Issue: 3 Linguagem: Inglês

10.1124/jpet.109.152801

1521-0103

Jand Venes Rolim Medeiros, Victor Hugo Braz Bezerra, Antoniella S. Gomes, André Luiz dos Reis Barbosa, Roberto César Pereira Lima‐Júnior, Pedro Marcos Gomes Soares, Gerly Anne de Castro Brito, Ronaldo A. Ribeiro, Fernando Q. Cunha, Marcellus Henrique Loiola Ponte de Souza,

Neuroscience of respiration and sleep

The aim of this study was to evaluate the protective effect of hydrogen sulfide (H 2 S) on ethanol-induced gastric lesions in mice and the influence of ATP-sensitive potassium (K ATP ) 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 Lawesson9s 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 Lawesson9s 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 Lawesson9s reagent treatment prevented ethanol-induced macroscopic and microscopic gastric damage in a dose-dependent manner. Administration of propargylglycine, an inhibitor of endogenous H 2 S synthesis, reversed gastric protection induced by l-cysteine. Glibenclamide reversed l-cysteine, NaHS, or Lawesson9s 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 H 2 S donors (NaHS or Lawesson9s reagent) in ethanol-induced macroscopic gastric damage. Likewise, in the presence of the TRPV1 antagonist capsazepine, the gastroprotective effects of l-cysteine, NaHS, or Lawesson9s reagent were also abolished. Our results suggest that H 2 S 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 K ATP channels and afferent neurons/TRPV1 receptors is of primary importance.