[Interaction of Helicobacter polyri and indomethacin in gastric mucosa injury of Balb/c mice].

Zhonghua Yi Xue Za Zhi

Department of Gastroenterology, Peking University Hospital, Beijing 100034, China.

Published: May 2003

AI Article Synopsis

  • The study aims to explore how Helicobacter pylori (Hp) interacts with indomethacin to cause gastric mucosa damage in Balb/c mice.
  • Fifty mice were divided into five groups, each receiving different treatments involving Hp inoculation and indomethacin injections, and were observed for gastric injury after four weeks.
  • Results showed a 66.7% infection rate among Hp-infected mice, with significant inflammation noted in group A, indicating a strong correlation between Hp and indomethacin in causing gastric injury.

Article Abstract

Objective: To investigate the interaction of Helicobacter pylori (Hp) and indomethacin in gastric mucosa injury of Balb/c mice.

Methods: Fifty specific pathogen free 6-week-old Balb/c mice were randomly divided into 5 groups: group A (n = 8, 25 mg/kg indomethacin was injected intraperitoneally every other day for 6 times, and 0.2 ml Hp culture containing 1 x 10(8) - 1 x 10(9) CFU/ml was inoculated intra-gastrically every other day for 6 times), B (n = 8, 1 x 10(8) - 1 x 10(9) CFU/ml Hp culture was inoculated intra-gastrically on the 1st, 2nd, and 3rd days, and since the 7th day 25 mg/kg indomethacin was injected intraperitoneally every other day for 6 tomes), group C (n = 9, 0.2 ml normal saline was inoculated intra-gastrically on the 1st, 2nd, and 3rd days and since the 7th day 25 mg/kg indomethacin was injected intraperitoneally every other day for 6 times), group D (n = 10, 1 x 10(8) - 1 x 10(9) CFU/ml Hp culture was inoculated intra-gastrically on the 1st, 2nd, and 3rd days, and since the 7th day 0.2 ml normal saline was injected intraperitoneally every other day for 6 times), and group E (n = 10, 0.2 ml normal saline was inoculated intra-gastrically on the 1st, 2nd, and 3rd days, then 0.2 ml normal saline was injected intraperitoneally since the 7th day every other day for 6 times). The mice were killed in the 4th week. The stomachs were observed morphologically. Tissues from gastric antrum underwent HE staining, silver staining, and urease examination. Rauws classification was used to grade the gastritis thus discovered.

Results: Two mice in group A, one mouse in group B and 2 mice in group C died. One mouse in group B was Hp silver staining negative. Twenty-six of the total 30 mice infected with Hp showed inflammation with an infection rate of 66.7%. Moderate to severe inflammatory reaction was seen in all 8 mice in group A with an average gastritis score of 6.38 and with Hp found in the epithelium. Two out of the 8 mice in group showed focal erosion. All mice in group B showed moderate inflammation and Hp in mucosa with an average gastritis score of 5.13. Focal erosion was seen in one mouse in group B. Light moderate inflammation was seen in all 9 mice in group C with an average gastritis score of 3.89. Mild inflammation was seen in all 10 mice in group D with an average gastritis score of 2.8. No erosion was found in groups C and D. No inflammation was seen in the mice in group E with an average gastritis score of 0.4. The differences between any 2 groups were all significant.

Conclusion: Hp and indomethacin synergetically aggravate the gastric epithelial injury. Prior Hp infection may be a protective factor of indomethacin-induced gastritis to a certain degree.

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