beraprost and Stomach-Ulcer

beraprost has been researched along with Stomach-Ulcer* in 2 studies

Other Studies

2 other study(ies) available for beraprost and Stomach-Ulcer

ArticleYear
Adaptive HNE-Nrf2-HO-1 pathway against oxidative stress is associated with acute gastric mucosal lesions.
    American journal of physiology. Gastrointestinal and liver physiology, 2008, Volume: 295, Issue:3

    Disturbance of the microcirculation and generation of reactive oxygen species are crucial in producing acute gastric mucosal lesions (AGML). To understand the protective mechanism against mucosal injury and oxidative stress in the stomach, we investigated sequential expression and localization of a product of lipid peroxidation and a chemical mediator of the oxidative response array, 4-hydroxynonenal (HNE), transcriptional factor, NF-E2-related factor (Nrf2), and the inducible heme oxygenase (HO-1) in the injured stomach. AGML was produced by intragastric administration of 0.6 N HCl in male rats. Expression and localization of HNE, Nrf2, and HO-1 were investigated by Western blotting, immunohistochemistry, real-time RT-PCR, and in situ hybridization histochemistry. Mucosal lesions and expression of HNE and HO-1 were assessed by prior treatment with the PGI2 analog beraprast or after sensory denervation by pretreatment with capsaicin. Mucosal lesions were assessed by prior treatment with a HO-1 inhibitor, zinc protoporphyrin (ZnPP). After AGML, increased generation of HNE was observed in the injured mucosa and the surrounding submucosa, followed by nuclear translocation of Nrf2 and upregulation of HO-1 in the macrophages located in the margin of the injured mucosa and in the submucosa. Pretreatment with beraprost attenuated AGML and downregulated the expression of HNE and HO-1, while sensory denervation aggravated AGML and upregulated the expression of HNE and HO-1. Pretreatment with ZnPP also aggravated AGML. The sequential HNE-Nrf2-HO-1 pathway in the gastric mucosal cells and the macrophages is involved in an adaptive mechanism against oxidative stress after AGML.

    Topics: Adaptation, Physiological; Aldehydes; Animals; Capsaicin; Cytoprotection; Denervation; Disease Models, Animal; Enzyme Inhibitors; Epoprostenol; Gastric Mucosa; Heme Oxygenase (Decyclizing); Hydrochloric Acid; Lipid Peroxidation; Macrophages; Male; NF-E2-Related Factor 2; Oxidative Stress; Protoporphyrins; Rats; Rats, Wistar; Signal Transduction; Stomach Ulcer

2008
Effect of a prostaglandin I2 analogue, beraprost sodium, on burn-induced gastric mucosal injury in rats.
    Burns : journal of the International Society for Burn Injuries, 1997, Volume: 23, Issue:3

    Stress ulcers still have a high mortality in critically burned patients and the pathophysiology remains relatively unknown. Impaired gastric mucosal perfusion is one of the factors contributing to gastric mucosal ulceration. Burn injury causes thrombosis and vascular occlusion by increasing the blood viscosity, resulting in decreased organ perfusion. Reduced blood flow is one of the most important factors in gastric mucosal ulceration. Beraprost sodium is a chemically stable prostaglandin I2 (PGI2) analogue with antiplatelet, vasodilator and cytoprotective actions. In the present study, we examined the effects of a PGI2 analogue, beraprost sodium (Procylin, Kaken Pharmaceutical Company, Tokyo, Japan) on burn-induced gastric mucosal changes in rats. Twenty male Sprague-Dawley rats weighing an average of 400 g were burned with hot water (90 degree C) and then divided into two groups of 10 animals. One group received 0.015 mg of beraprost sodium intraperitoneally immediately after burn injury, while the control group received the same volume of saline. Gastric mucosal blood flow was measured with a laser Doppler flowmeter and the area of mucosal necrosis was also determined macroscopically and histologically. Gastric mucosal damage was significantly reduced in the beraprost sodium-treated rats and gastric mucosal blood flow was significantly improved (p < 0.05). These findings demonstrate that PGI2 plays a very important role in the pathophysiology of burn-induced Curling's ulcer and that beraprost sodium can improve gastric mucosal blood flow and reduce mucosal damage.

    Topics: Animals; Blood Flow Velocity; Burns; Disease Models, Animal; Epoprostenol; Gastric Mucosa; Laser-Doppler Flowmetry; Male; Platelet Aggregation Inhibitors; Rats; Rats, Sprague-Dawley; Stomach Ulcer; Stress, Physiological; Vasodilator Agents

1997