ArticleFrontiers in cellular and infection microbiology2025
Indole-3-carboxamide alleviates LPS-induced endometritis through suppressing ferroptosis and inflammation via regulating Aryl hydrocarbon receptor.
Article in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Indole-3-carboxamide (I3A), a derivative of tryptophan indole, has been reported to have anti-inflammatory role. This study aims to investigate the effects of I3A on LPS-induced endometritis in mice. Methods: The mice endometritis model was established and I3A was administered to mice orally (150 mg/kg/day) for two days. TNF-α and IL-1β production were analyzed by ELISA. The protein expression was measured by western blot. The pathological changes of mouse uterine tissue were observed by H&E staining. Results: The experimental results showed I3A significantly alleviated LPS-induced uterine pathological injury. I3A treatment obviously attenuated LPS-induced MPO activity, TNF-α and IL-1β production. I3A also inhibited LPS-induced ferroptosis and NF-κB activation. Furthermore, I3A could up-regulate the expression of AhR and SLC7A11. The protective role of I3A on LPS-induced endometritis was reversed by AhR inhibitor CH223191. Conclusion: In conclusion, I3A inhibits LPS-induced endometritis in mice by attenuating inflammation and ferroptosis via the AhR-SLC7A11 signaling pathway.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.