ArticleDie Naturwissenschaften2025
Gamma-aminobutyric acid attenuates cortisol-induced damage in human colorectal adenocarcinoma cells via Nrf2 signaling.
Article in Die Naturwissenschaften, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Dietary Rumen-Protected Gamma-Aminobutyric Acid Supplementation to Alleviate Stress in Beef Cattle Caused by Long-Distance Transport by Improving Antioxidant Capacity, Immune Function, and Hormonal Balance: A Related Study.Animals : an open access journal from MDPI · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term psychological stress is associated with increased intestinal epithelial permeability. In the human central nervous system, gamma-aminobutyric acid (GABA), a non-protein amino acid found in bacteria, plants, and animals, acts as an inhibitory neurotransmitter that controls the cardiovascular system, reduces blood pressure, enhances mood, and encourages sleep. It is still unclear how GABA controls the function of the colon epithelial barrier under long-term stress. This study explored the potential of GABA to ameliorate cortisol-induced damage in human colorectal adenocarcinoma cells (HT29) and the mechanisms at play. Our results indicate that GABA mitigated cellular damage by neutralizing the negative impacts of Cortisol on HT29 cell viability, permeability, and the expression of barrier-associated proteins. Additionally, GABA maintained the cellular barrier function and antioxidant defense. Overall, our results point to the possibility that GABA may shield HT29 cells from harm caused by cortisol by activating the Nrf2 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.