ArticleInflammopharmacology2003
Differential role of platelet-activating factor in gastric mucosal ulcer healing.
Article in Inflammopharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- TNFα promotes mucosal wound repair through enhanced platelet activating factor receptor signaling in the epithelium.Mucosal immunology · 2019Article
- Treatment Effects of Jinlingzi Powder and Its Extractive Components on Gastric Ulcer Induced by Acetic Acid in Rats.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Macrophage derived platelet activating factor implicated in the resolution phase of gouty inflammation.International journal of inflammation · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelet-activating factor (PAF) is a potent phospholipid-derived messenger involved in a number of diverse pathological conditions, including mediation of inflammatory cascades associated with wound healing. In this study, we investigated the effect of a specific PAF antagonist, BN52020, on the course of experimentally induced gastric mucosal ulcer healing by analyzing apoptotic processes and the mucosal expression of TNF-alpha, COX-2, and the activity of inducible nitric oxide synthase (NOS-2). Groups of rats were intragstrically pretreated with BN52020 either 24 and 4 h before acetic acid injury (prophylactic) or 24 and 44 h after the injury (therapeutic) and their mucosal tissue subjected to assessment of ulcer healing rate and biochemical measurements. Compared with the controls, the prophylactic administration of BN52020 produced dose-dependent acceleration in ulcer healing, accompanied by an increase in COX-2 expression and a marked reduction in the extent of mucosal apoptosis, TNF-alpha and NOS-2 activity. A delay in ulcer healing, however, occurred with BN52020 administered therapeutically, and this effect of the agent was reflected in a decreased COX-2 protein expression and a significant increase in the rate of epithelial cell apoptosis, TNF-alpha, and the mucosal NOS-2 activity. Thus, PAF antagonist, BN52020, when administered prophylactically exerts anti-inflammatory effects that accelerate gastric ulcer healing, while given therapeutically interferes with COX-2 enzyme expression that leads to a protracted inflammatory responses that delay ulcer healing.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.