Table 1.

The effects of H₂S in gastric mucosa damage

Study	Model	Animals/cells	Main results
Aboubakr et al.29	CRS	Rats	NaHS (60 μmol/kg, intraperitoneal injection) reduced the serum level of TNF-α and myeloperoxidase activity, and abrogated the inflammatory and the deleterious responses of gastric mucosa in CRS.
Guo et al.28	Ischemic eperfusion	Human gastric epithelial cell	H2S exerted its protective effect through reactive oxygen species clearance, inhibition of p38 and JNK dependent cell apoptosis and NF-κB dependent inflammation pathway.
Magierowski et al.31	Acetic acid	Rats	NaHS (10 mg/kg, intragastric administration) significantly decreased ulcer area and increased GBF at ulcer margin.
Magierowski et al.30	NSAIDs	Rats	NaHS (5 mg/kg, intragastric administration) could raise mRNA or protein expression for CSE, COX-1 and decreased mRNA expression for IL-1β level in blood.
Magierowski et al.34	WRS	Rats	NaHS dose-dependently attenuated severity of WRS-induced gastric lesions, increased GBF and improve gastric microcirculation.
Medeiros et al.26	Ethanol	Mice	NaHS and Lawesson’s reagent (donors of H2S) decreased hemorrhagic damage, edema and epithelial cell loss.
Sun et al.27	WRS	Rats	H2S played a protective role against WRS-induced gastric mucosal injury in rats, possibly through modulation of K+ATP channel opening and through the NF-κB dependent pathway.

Note: H₂S: Hydrogen sulfide; CRS: cold restraint stress; NaHS: sodium hydrosulfide; TNF-α: tumor necrosis factor-α; GBF: gastric blood flow; NSAIDs: non-steroidal anti-inflammatory drugs; CSE: cystathionine-γ-lyase; COX-1: cyclooxygenase-1; IL-1β: interleukin-1β; WRS: water immersion and restraint stress; JNK: c-Jun N-terminal kinase; NF-κB: nuclear factor-κB; K⁺ATP: ATP-sensitive potassium.