ArticleInflammation2026
GTS-21 Alleviates Acute Lung Injury by Enhancing GLP-1 Secretion and Regulating Alveolar Surfactant Proteins via α7nAChR Activation.
Article in Inflammation, 2026. 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
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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.
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Who cites it
1 citing paper in PubMed.
- Discovery of a novel cannabidiol-derived transient receptor potential vanilloid 4 inhibitor to reduce pulmonary edema and lung vascular permeability in mice.Cellular & molecular biology letters · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
GTS-21, a selective α7-nicotinic acetylcholine receptor (α7nAChR) agonist, exhibits significant anti-inflammatory effects in acute lung injury (ALI), but its mechanisms remain incompletely understood. We hypothesize that its protective effects involve the regulation of Glucagon-like peptide-1 (GLP-1) and pulmonary surfactant protein (SP). P. aeruginosa-induced pneumonia (2.5 × 10⁵ CFU/mouse) and LPS-induced ALI (2.5 mg/kg) models via intratracheal instillation (IT) were used in WT, α7nAChR KO and GLP-1R KO mice. Lung injury was assessed via histopathology, cytokine quantification (IL-6, HMGB1), alveolar–capillary barrier injury, immune cell infiltration, circulating GLP-1, and SP expression in bronchoalveolar lavage fluid (BALF). GTS-21 significantly reduced mortality in WT mice with P. aeruginosa pneumonia, while α7nAChR KO mice showed increased mortality. GTS-21 also improved survival, attenuated lung injury, decreased leukocyte infiltration, and reduced HMGB1/protein concentration in BALF. In murine lipopolysaccharide (LPS)-induced ALI, GTS-21 improved histopathology and alveolar–capillary barrier integrity, lowered IL-6 and HMGB1, and enhanced GLP-1 elevation in WT mice but not α7nAChR KO mice. Furthermore, LPS suppressed SP-A and SP-D in BALF, which GTS-21 restored in WT mice. To confirm the role of GLP-1 in GTS-21-mediated lung protection, we examined inflammation in GLP-1R KO mice following LPS challenge. Anti-inflammatory effects of GTS-21 were blunted in these mice, suggesting a GLP-1-dependent mechanism. GTS-21 protects against bacterial pneumonia and ALI through α7nAChR activation, GLP-1 modulation, and SP regulation. These findings provide evidence that the protective effects of GTS-21 on ALI are mediated in part by GLP-1 and pulmonary surfactant.
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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.