Component
Gastroduodenal mucosal defence
Gastroduodenal mucosal defence. Species, exposure and limitations are retained in each linked claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
Where it participates (unsigned role)
A range of non-steroidal anti-inflammatory agents including acetylsalicylic acid, fenclofenac, ibuprofen and indomethacin inhibit gastric bicarbonate transport in isolated mucosal preparations, effects which can be antagonised by exogenous prostaglandins of the E series, and while the secreted mucus gel overlying the epithelial surface is not affected in the short term a number of these agents inhibit glycoprotein biosynthesis by the epithelial cells, so that loss of this protective coat could be anticipated during chronic exposure as erosion by luminal shear and proteolysis would not be compensated by continued secretion.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/ibuprofen-research/3303291.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8609926e51d2ad349198eb5f3ad78b6b552e8f4d4fc74d07bb3a58795a86e7a7", "start_char": 0, "end_char": 1757, "text_sha256": "8609926e51d2ad349198eb5f3ad78b6b552e8f4d4fc74d07bb3a58795a86e7a7"}
- experimental_model
- Review of gastroduodenal defence with isolated mucosal preparations
- exposure
- Acetylsalicylic acid, fenclofenac, ibuprofen and indomethacin on bicarbonate transport and glycoprotein synthesis
- limitations
- A review of mechanisms rather than an outcome study. The claim that E-series prostaglandins reverse the effect is what ties it to cyclooxygenase.
- nutrient_topic
- Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
- organism
- Human and animal
- plain_language
- The stomach’s own defences are built by prostaglandins, so blocking them removes the coat rather than adding an acid.
- primary_references
- [ibu-p3303291] Gastroduodenal mucosal defence mechanisms and the action of non-steroidal anti-inflammatory agents. (1987). https://pubmed.ncbi.nlm.nih.gov/3303291/ DOI: 10.3109/00365528709090947
- tissue_or_cell_type
- Gastric and duodenal mucosa
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of gastroduodenal defence with isolated mucosal preparations · source_derived_draft · unverified_draft
### ibu-bicarbonate-and-mucus A range of non-steroidal anti-inflammatory agents including acetylsalicylic acid, fenclofenac, ibuprofen and indomethacin inhibit gastric bicarbonate transport in isolated mucosal preparations, effects which can be antagonised by exogenous prostaglandins of the E series, and while the secreted mucus gel overlying the epithelial surface is not affected in the short term a number of these agents inhibit glycoprotein biosynthesis by the epithelial cells, so that loss of this protective coat could be anticipated during chronic exposure as erosion by luminal shear and proteolysis would not be compensated by continued secretion. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: The stomach’s own defences are built by prostaglandins, so blocking them removes the coat rather than adding an acid. organism: Human and animal tissue_or_cell_type: Gastric and duodenal mucosa experimental_model: Review of gastroduodenal defence with isolated mucosal preparations limitations: A review of mechanisms rather than an outcome study. The claim that E-series prostaglandins reverse the effect is what ties it to cyclooxygenase. exposure: Acetylsalicylic acid, fenclofenac, ibuprofen and indomethacin on bicarbonate transport and glycoprotein synthesis evidence_span: {"source_cache": "artifacts/ibuprofen-research/3303291.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8609926e51d2ad349198eb5f3ad78b6b552e8f4d4fc74d07bb3a58795a86e7a7", "start_char": 0, "end_char": 1757, "text_sha256": "8609926e51d2ad349198eb5f3ad78b6b552e8f4d4fc74d07bb3a58795a86e7a7"} [ibu-p3303291] Gastroduodenal mucosal defence mechanisms and the action of non-steroidal anti-inflammatory agents. (1987). https://pubmed.ncbi.nlm.nih.gov/3303291/ DOI: 10.3109/00365528709090947
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.