ArticleArchives of medical science : AMS2023
γ-aminobutyric acid alleviates LPS-induced acute lung injury in mice through upregulating type B receptors.
Article in Archives of medical science : AMS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- In silico pharmacology and 3D-bioprinting reveal Dicranum scoparium as an inhibitor of NF-κB-induced inflammation in the 3D4/31 alveolar macrophage cell line.Journal of natural medicines · 2026Article
- GABA Prevents Sarcopenia by Regulation of Muscle Protein Degradation and Inflammaging in 23- to 25-Month-Old Female Mice.Journal of cachexia, sarcopenia and muscle · 2024Article
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
Introduction: In recent years, studies have shown that GABA has a certain therapeutic effect on acute lung injury (ALI), but its specific mechanism has not been fully elucidated. The study was designed to investigate the protective effect and mechanism of γ-aminobutyric acid (GABA) on ALI induced by lipopolysaccharide (LPS) in mice. Material and methods: C57BL/6 mice were randomly divided into a control group, LPS group, LPS + GABA (10 mg/kg) group and LPS + dexamethasone (Dex, 5 mg/kg) group. The survival rate of each group was observed at different time points after modeling. The levels of tumor necrosis factor α (TNF-α), interleukin (IL) 1β, 10, myeloperoxidase (MPO) and the cell count and protein concentration in bronchoalveolar lavage fluid (BALF) were measured. Lung histopathology and the expression of GABA receptors were observed by HE staining and immunohistochemistry respectively. Lung water content was assessed by wet-dry weight ratio. Results: GABA could significantly improve the survival rate and prolong the survival time of animals, alleviate the degree of inflammatory injury and pulmonary edema, reduce the content of MPO, down-regulate the levels of pro-inflammatory cytokines IL-1β and TNF-α, and up-regulate the expression of anti-inflammatory cytokine IL-10. Moreover, GABA could significantly decrease the expression of type A receptors and enhance type B receptors. Conclusions: GABA can effectively alleviate ALI induced by LPS in mice, and its effect may be related to the upregulation of type B receptors.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.