Chronic Administration with Electrolyzed Alkaline Water Inhibits Aspirin-induced Gastric Mucosal Injury in Rats through the Inhibition of Tumor Necrosis Facter-.ALPHA. Expression

Abstract:

Neutrophils activation and tumor necrosis factor-α (TNF-α) induction play critical roles in aspirin-induced gastric mucosal injury. The aim of the present study was to determine whether electrolyzed alkaline water (EAW) can ameliorate aspirin-induced gastric mucosal injury in rats, and whether EAW can inhibit the increased gastric TNF-α expression associated with neutrophil accumulation and gastric epithelial cell apoptosis. EAW (pH 10.5, oxidation-reduction potential -450mW) was produced by electricity resolution of tap water with a device that used a platinum electrode. EAW was administered to rats via free drinking for 14 days. Aspirin-induced injury was produced by the intragastric administration of aspirin (200mg/kg) and HCl (0.15N, 8.0ml/kg). After 3h the animals were killed, and the gastric mucosal tissue was used for the assessment of macroscopic damage and tissue-associated myeloperoxidase (MPO) activity, the quantitation of TNF-α protein, and the assay of epithelial cell apoptosis. The expression of TNF-α mRNA was determined by reverse transcription polymerase chain reaction (RT-PCR) 1h after aspirin administration. In the group drinking tap water, intragastric administration of acidified aspirin induced hyperemia and hemorrhagic erosions in rat stomachs. The increase in the total gastric erosive area after aspirin administration was significantly inhibited by pretreatment with EAW. The increases in MPO activity and epithelial cell apoptosis after aspirin administration were significantly inhibited by treatment with EAW. The gastric content of TNF-α increased and the expression of TNF-α mRNA was up-regulated after aspirin treatment. However, the peak TNF-α mRNA expression 1h after aspirin administration was inhibited by EAW. Based on these data, we conclude that the beneficial effects of EAW on aspirin-induced gastric mucosal injury may be attributed to its anti-inflammatory properties via inhibition of TNF-α expression.