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Inflammation Research

, Volume 58, Issue 10, pp 717–723 | Cite as

Lipopolysaccharide from Escherichia coli prevents indomethacin-induced gastric damage in rats: role of non-protein sulfhydryl groups and leukocyte adherence

  • Antoniella Souza Gomes
  • Henrique Paula Lemos
  • Jand Venes Rolim Medeiros
  • Fernando Queiroz Cunha
  • Marcellus Henrique Loiola Ponte Souza
Original Research Paper

Abstract

Objective and design

To investigate the role of non-protein sulfhydryl groups (NP-SH) and leukocyte adhesion in the protective effect of lipopolysaccharide (LPS) from Escherichia coli against indomethacin-induced gastropathy.

Materials or subjects

Male Wistar rats were divided into four groups: saline, LPS, saline + indomethacin and LPS + indomethacin, with six rats in each group.

Treatment

Rats were pretreated with LPS (300 μg/kg, by intravenous) or saline. After 6 h, indomethacin was administered (20 mg/kg, by gavage).

Methods

Three hours after treatments, rats were killed. Macroscopic gastric damage, gastric NP-SH concentration, myeloperoxidase (MPO) activity and mesenteric leukocyte adhesion (intravital microscopy) were assessed. Statistical analysis was performed using one-way analysis of variance followed by the Newman–Keuls test. Statistical significance was set at P < 0.05.

Results

LPS reduced the gastric damage, gastric MPO activity and increased gastric NP-SH concentration in indomethacin-induced gastropathy. LPS alone increased gastric NP-SH when compared to saline. Indomethacin increased leukocyte adhesion when compared to the saline, and LPS reduced indomethacin-induced leukocyte adhesion. In addition, LPS alone did not change leukocyte adhesion, when compared to the saline.

Conclusion

LPS protective effect against indomethacin-induced gastropathy is mediated by an increase in the NP-SH and a decrease in leukocyte–endothelial adhesion.

Keywords

LPS GI damage NSAIDs Leukocyte adhesion 

Abbreviations

LPS

Lipopolysaccharide

NSAIDs

Non-steroidal anti-inflammatory drugs

INDO

Indomethacin

NO

Nitric oxide

NOS

Nitric oxide synthase

iNOS

Inducible nitric oxide synthase

MPO

Myeloperoxidase

NP-SH

Non-protein sulfhydryl groups

Notes

Acknowledgments

The authors gratefully acknowledge the technical assistance of Maria Silvandira Freire França. Grants from CNPq (Brazil) supported this work. Dr. Cunha and Dr. Souza are recipients of a CNPq fellowship. This work is part of the requirements to obtain a Master of Science degree in Pharmacology at the School of Medicine, Federal University of Ceara by one of us (A.S. Gomes).

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Copyright information

© Birkhäuser Verlag, Basel/Switzerland 2009

Authors and Affiliations

  • Antoniella Souza Gomes
    • 1
  • Henrique Paula Lemos
    • 2
  • Jand Venes Rolim Medeiros
    • 1
  • Fernando Queiroz Cunha
    • 2
  • Marcellus Henrique Loiola Ponte Souza
    • 1
  1. 1.Department of Physiology and Pharmacology, School of MedicineFederal University of CearáFortalezaBrazil
  2. 2.Department of Pharmacology, Ribeirão Preto School of MedicineUniversity of Sao PauloRibeirão PrêtoBrazil

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