- Protect rat gastric mucosa against CRS-induced gastric ulceration through anti-oxidant and anti-inflammatory actions alongside enhancement of gastric mucosal barrier and reduction in acid secretory parameters.1
- H₂S prodrugs significantly increased the extent of healing of gastric ulcers as compared to vehicle-treatment. These results suggest that H₂S is produced in the gastric mucosa in response to injury and acts to promote healing. The results further suggest that drugs releasing hydrogen sulfide could be employed to accelerate healing of gastric ulcers, and possibly of other wounds.2
- Pre-exposure to H₂S significantly reduced the gastric ulcer index, in WRS rats. Pre-exposure to H₂S markedly suppressed plasma ACTH and corticosterone level by 34.4 and 53.2%, respectively (both P < 0.01), and reduced WRS-elevated myeloperoxidase (MPO) activity by 19%. H₂S exposure reduced lipid peroxide production and inhibited the WRS-elevated expression of glucose-regulated protein 78 and caspase 12, markers of endoplasmic reticulum stress.3
- Garlic compound DADS reduced peptic ulcer H. pylori growth and NAT activity.4
- Gaseous mediators nitric oxide and hydrogen sulfide in the mechanism of gastrointestinal integrity, protection and ulcer healing.
H₂S reduced the severity of esophageal injury and inflammation and normalized the serum cytokine levels in rat erosive esophagitis; H₂S contributes significantly to mucosal defence in the esophagus, and H₂S donors may have therapeutic value in treating esophageal inflammation and injury.5