Alkaline Water Protects Stomach from Aspirin Damage in Rats
- Authors
- Yuji Naito, Tomohisa Takagi, Kazuhiko Uchiyama, Naoya Tomatsuri, Kiichi Matsuyama, Takaaki Fujii, Nobuaki Yagi, Norimasa Yoshida, Toshikazu Yoshikawa
- Journal
- Journal of Clinical Biochemistry and Nutrition
- Year
- 2002
- DOI
- 10.3164/jcbn.32.69
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Aspirin-induced Gastropathy
- Body System
- Digestive
TL;DR
Drinking electrolyzed alkaline water (EAW) can reduce stomach damage and inflammation caused by aspirin in rats.
Key Finding
In rats, electrolyzed alkaline water reduced aspirin-induced stomach damage and suppressed TNF-α expression, a key inflammatory protein involved in gastric injury.
Summary
Researchers gave rats electrolyzed alkaline water (water treated with electricity to increase pH and change its chemical properties) for 14 days, then exposed them to aspirin and acid to simulate stomach damage. Rats that drank the alkaline water had significantly less stomach damage, less inflammation, and lower levels of TNF-α (a protein that triggers inflammation) compared to rats drinking regular tap water. The study suggests the alkaline water's protective effect comes from reducing inflammatory responses in the stomach.
Practical Takeaway
This is an animal study only, so results cannot be directly applied to humans. While the findings suggest electrolyzed alkaline water may have anti-inflammatory properties in the stomach, much more research—including human trials—would be needed before recommending it as a protective measure for people taking aspirin long-term. The study does not establish whether regular hydrogen water or alkaline water would have similar effects in humans.
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.