H. Suzuki et al., Polaprezinc attenuates the Helicobacter pylori-induced gastric mucosal leucocyte activation in Mongolian gerbils - a study using intravital videomicroscopy, ALIM PHARM, 15(5), 2001, pp. 715-725
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.