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Possible protective effect of TNF-α inhibition and triad NO/cGMP/VEGF activation on gastric ulcer in rats.

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  • Additional Information
    • Source:
      Publisher: Canadian Science Publishing Country of Publication: Canada NLM ID: 0372712 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1205-7541 (Electronic) Linking ISSN: 00084212 NLM ISO Abbreviation: Can J Physiol Pharmacol Subsets: MEDLINE
    • Publication Information:
      Publication: 2011- : Ottawa, ON : Canadian Science Publishing
      Original Publication: Ottawa, National Research Council of Canada.
    • Subject Terms:
      Cyclic GMP/*physiology ; Nitric Oxide/*physiology ; Stomach Ulcer/*drug therapy ; Tumor Necrosis Factor-alpha/*antagonists & inhibitors ; Vascular Endothelial Growth Factor A/*physiology; Animals ; Dinoprostone/blood ; Indomethacin/toxicity ; Male ; Malondialdehyde/analysis ; Pentoxifylline/therapeutic use ; Rats ; Stomach Ulcer/pathology ; Tadalafil/therapeutic use ; Tumor Necrosis Factor-alpha/analysis ; Vascular Endothelial Growth Factor A/analysis
    • Abstract:
      Peptic ulcers are one of the world's major gastrointestinal disorders, embracing both gastric and duodenal ulcers, and affecting 10% of the world population. The current study aimed to investigate the possible protective effect of tadalafil and pentoxifylline (PTX) on indomethacin-induced peptic ulcers. Male albino rats were divided into five groups: control group; ulcerated group; Indomethacin + Tadalafil, in which animals were pretreated with tadalafil orally before indomethacin; Indomethacin+ PTX, in which animals were pretreated with PTX orally before indomethacin; and Indomethacin + Tadafil + PTX. Indomethacin treatment revealed histopathological changes and ulcer scoring and ulcer index were markedly increased. Serum levels of prostaglandin and heme oxygenase-1 were significantly decreased. The ulcerogenic also induced marked oxidative stress as evident from the increased malondialdehyde, decreased in gastric glutathione content and superoxide dismutase activity, while the gastric myeloperoxidase was increased. Gastric nitric oxide content was decreased and the expression of vascular endothelial growth factor was downregulated while the tumor necrosis factor α (TNF-α) level was dramatically increased. Pretreatment of the ulcerative group by either tadalafil or PTX or their combination improved all these pathological changes. Tadalafil or PTX may have a role in protecting gastric mucosa damage caused by indomethacin which may be useful in the future for the treatment of gastric ulceration.
    • Contributed Indexing:
      Keywords: gastric ulcer; indomethacin; indométacine; pentoxifylline; pentoxiphylline; tadalafil; ulcère gastrique
    • Accession Number:
      0 (Tumor Necrosis Factor-alpha)
      0 (Vascular Endothelial Growth Factor A)
      31C4KY9ESH (Nitric Oxide)
      4Y8F71G49Q (Malondialdehyde)
      742SXX0ICT (Tadalafil)
      H2D2X058MU (Cyclic GMP)
      K7Q1JQR04M (Dinoprostone)
      SD6QCT3TSU (Pentoxifylline)
      XXE1CET956 (Indomethacin)
    • Publication Date:
      Date Created: 20210105 Date Completed: 20220117 Latest Revision: 20220117
    • Publication Date:
      20250114
    • Accession Number:
      10.1139/cjpp-2020-0725
    • Accession Number:
      33400612