Effect of vitamin C-releasing acetylsalicylic acid on gastric mucosal damage before and after Helicobacter pylori eradication therapy.
The interaction between Helicobacter pylori (H. pylori) and nonsteroidal anti-inflammatory drugs (NSAIDs) such as acetylsalicylic acid is still controversial. This study was designed to compare the effect of acetylsalicylic acid and vitamin C-releasing acetylsalicylic acid on the gastric mucosal damage and microbleeding before and after eradication of H. pylori in 10 young healthy volunteers. Acetylsalicylic acid induced significantly more gastric lesions and higher microbleeding than acetylsalicylic acid-vitamin C. After successful H. pylori eradication therapy, acetylsalicylic acid induced significantly higher mucosal lesions and microbleeding than before eradication. In contrast, after acetylsalicylic acid-vitamin C, gastric lesion index was significantly lower and eradication therapy failed to aggravate it. All H. pylori-positive subjects showed significant up-regulation of antioxidant enzyme (superoxide dismutase, catalase, glutathione peroxidase). Plain acetylsalicylic acid stronger than acetylsalicylic acid-vitamin C reduced gastric gene expression of these antioxidant enzymes. H. pylori eradication significantly decreased expression of these enzymes and this was further enhanced by plain acetylsalicylic acid, but not acetylsalicylic acid-vitamin C. Under plain acetylsalicylic acid therapy, the expression of proinflammatory cytokines was increased before and after eradication of H. pylori. We conclude that vitamin C combined with acetylsalicylic acid, unlike plain acetylsalicylic acid without vitamin C, protects gastric mucosa in man probably due the attenuation of oxidative stress and proinflammatory cytokines.
Konturek
Peter C
PC
First Department of Medicine, University Erlangen-Nuremberg, Germany.
Kania
Joanna
J
Gessner
Uwe
U
Konturek
Stanisław J
SJ
Hahn
Eckhart G
EG
Konturek
Jan W
JW
D000293:Adolescent; D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology*; D015153:Blotting, Western; D002374:Catalase / Q000096:biosynthesis / Q000235:genetics; D016207:Cytokines / Q000378:metabolism; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology*; D006471:Gastrointestinal Hemorrhage / Q000473:pathology; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000096:biosynthesis / Q000235:genetics; D016481:Helicobacter Infections / Q000188:drug therapy / Q000473:pathology*; D006801:Humans; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000096:biosynthesis / Q000235:genetics; D052247:Nitric Oxide Synthase Type II; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013276:Stomach Ulcer / Q000473:pathology*; D013482:Superoxide Dismutase / Q000096:biosynthesis / Q000235:genetics
D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D016328:NF-kappa B; D002374:Catalase; D005979:Glutathione Peroxidase; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D013482:Superoxide Dismutase; D001205:Ascorbic Acid; D001241:Aspirin