Gastric mucosal inflammatory responses toHelicobacter pylori lipopolysaccharide: Suppression of caspase-3 and nitric oxide synthase-2 by omeprazole and sucralfate

Abstract

Our findings implicate caspase-3 involvement in gastric mucosal inflammatory responses toH. pylori lipopolysaccharide, and point towards participation of NOS-2 in the amplification of the cell death-signaling cascade. We also show that anti-ulcer agents, omeprazole and sucralfate, are capable of suppressing the H. pylori-induced mucosal inflammatory responses by interfering with the events propagated by NOS-2 and caspase-3.

Induction of Metastatic Gastric Cancer by Peroxisome Proliferator-Activated Receptorδ Activation

“…PPAR γ suppresses the growth and invasion of human colon [71] and gastric [72, 73] and esophageal carcinoma cells [74], and both PPAR γ [75] and PPAR α have anti-inflammatory actions [76]. Thus, reduction of PPAR α and PPAR γ expression may be an additional mechanism for facilitating the proinflammatory and tumor-promoting effects of GW501516.…”

Mucosal mRNA Cytokines’ Profile of Gastric Wall in Neonatal Foals: Comparison with Endoscopy and Histology

“…An experimental study in rats found that IL-4 had a rapid increase after the 4th day of the ulcer onset and remained high throughout the entire period of healing. The authors also stated that sucralfate, by eliciting rapid induction in IL-4 expression, was capable of efficient suppression of the mucosal apoptotic events, the cessation of which determined the efficiency of the healing process [39]. In a study about cytokine expression in pediatric H. pylori infection, IL-4 was present in both H. pylori infected and uninfected cases.…”

Gastritis Induced by Helicobacter pylori Infection in Experimental Rats

“…Gastric lesions can be also induced by necrotizing agents like acids, alkalies [16] and 80% ethanol [17,18]. Another model of gastritis can be induced by intragastric application of either H. pylori itself [19] or its lipopolysaccharides [20,21].…”