Ulcer was induced by oral administration of ethanol (75%, v/v) and indomethacin (50 mg/kg). Malondialdehyde, reduced glutathione and catalase activity was measured in stomach tissue after ethanol induced ulcer. In order to evaluate the effect of BI on nitric oxide, ulcer was induced by ethanol in l-NAME pretreated animals. Anti-Helicobacter pylori activity was verified in disk diffusion and broth microdilution in vitro assays, using cagA+ and vacA+ Helicobacter pylori strains.
BI prevented the gastric ulceration caused by ethanol and indomethacin treatments. Its gastroprotective mechanism in ethanol-induced ulcer was partly due to reduction of MDA and CAT levels in the gastric tissue. BI did not affect the GSH levels and its gastroprotective effect was not reversed by pretreatment with l-NAME. BI showed anti-Helicobacter pylori in the both assays.
The results indicate that BI is partly responsible for the HECb antiulcer and anti-Helicobacter pylori effects.