Polaprezinc attenuates the Helicobacter pylori-induced gastric mucosal leucocyte activation in Mongolian gerbils - a study using intravital videomicroscopy

Background: We previously demonstrated that Helicobacter pylori colonizatio n evokes gastric mucosal inflammation and an extensive increase in lipid pe roxides and glutathione in Mongolian gerbils. Zinc and its derivative, pola prezinc, have been reported to be potent antioxidants in gastric mucosa. Aim: To examine the effect of polaprezinc on gastric mucosal oxidative infl ammation in H. pylori-colonized Mongolian gerbils. Methods: Sixty-eight male Mongolian gerbils were orally inoculated with H. pylori (ATCC43504, 5 x 10(8) CFUs/gerbil; H. pylori group) and 35 gerbils w ere inoculated with the culture media (control group). Twenty-two gerbils i n the H. pylori and 13 gerbils in the control group were fed with diets con taining polaprezinc (0.06%, 100 mg/kg, 10 times the usual clinical dose) (H . pylori + polaprezinc group, polaprezinc group). The remaining gerbils wer e fed a standard laboratory chow diet. Neutrophil infiltration, assessed hi stologically and by the activity of myeloperoxidase, the contents of CXC-ch emokine (GR0/CINC-1-like protein) and the contents of thiobarbituric acid-r eactive substances, was evaluated in each group 12 weeks after the inoculat ion. Separately, gastric mucosal leucocyte activation and capillary perfusi on were also assessed using intravital microscopy 2, 4, 8 and 12 weeks afte r the inoculation. Results: In all H. pylori-inoculated animals, the bacterial infection persi sted throughout the experimental period. Gastric mucosal lesion formation i n the H pylori group was significantly inhibited in the H. pylori + polapre zinc group. Elevated levels of myeloperoxidase activity, GR0/ CINC-1 and th iobarbituric acid-reactive substances in the H. pylori group at 12 weeks we re attenuated significantly by polaprezinc treatment. Enhanced levels of ve nular leucocyte activation observed in the H. pylori group were attenuated significantly in the H. pylori + polaprezinc group during both the early ph ase (2 weeks) and late phase (12 weeks). Conclusion: Polaprezinc inhibited H. pylori-associated gastric mucosal oxid ative inflammation, including initial micro-vascular leucocyte activation, in Mongolian gerbils.