Diclofenac-induced gastric mucosal fluorescence in rats

We previously reported that the gastric mucosa emits fluorescence of porphy rins at the onset of gastric lesions induced by hemorrhagic shock. In this study, we investigated whether the fluorescent substance concerns with the gastric mucosal injuries induced by diflofenac, a nonsteroidal antiinflamma tory drug (NSAID). In the gastric mucosa treated with diclofenac, lesions w ere generated and myeloperoxidase activity increased. Diclofenac administra tion also increased thiobarbituric acid-reactive substances, a index of tis sue peroxidation. After diclofenac treatment, the gastric mucosal fluoresce nce intensities rose. HPLC analysis demonstrated that the fluorescent subst ances were mesoporphyrin and protoporphyrin, which were the same as found i n hemorrhagic shock. Pretreatment of the tissue with radical scavenging sub stances, catalase and troxipide, restrained the increase of mucosal fluores cence intensity, tissue peroxidation, and lesion formation. These findings indicate that diclofenac treatment induced the generation of porphyrins as well as tissue peroxidation in gastric mucosal tissue. This study suggests that autofluorescence observation is a useful tool to identify diclofenac-i nduced gastric injury.