ArticleMolecular neurobiology2026
Glaucocalyxin A Promotes Spinal Cord Repair By Nrf2/HO-1 Pathway Activation to Suppress AIM2 Inflammasome Formation.
Article in Molecular neurobiology, 2026. 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.
- Role of Pattern Recognition Receptors (PRRs) in Spinal Cord Injury (SCI): A Comprehensive Review.Molecular neurobiology · 2026Review
- Targeting Gasdermins for Therapeutic Interventions in Central Nervous System Injury.Neurotoxicity research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Spinal cord injury (SCI) is a debilitating neurological disorder that frequently results in severe motor, sensory, and autonomic dysfunction, often leading to permanent disability. However, due to the complexity of its pathophysiologic mechanisms, therapeutic options for SCI remain limited. In this study, we focus on Glaucocalyxin A (GLA), a bioactive diterpenoid compound derived from Lamiaceae plants, which exhibits remarkable anti-inflammatory and antioxidant properties and shows promising potential as a therapeutic candidate for SCI. This study aims to elucidate the mechanism by which GLA exerts its neuroprotective effects, namely by activating the Nrf2/HO-1 pathway to alleviate oxidative stress, thereby inhibiting absent in melanoma 2 (AIM2) inflammasome-mediated neuronal pyroptosis. This study employed network pharmacology and molecular docking to predict the therapeutic potential and mechanism of GLA in SCI. To validate these predictions, we established a rat SCI model to evaluate GLA's therapeutic effects. In vitro experiments were also conducted using lipopolysaccharide-stimulated PC12 cells to investigate GLA's neuroprotective effects against oxidative stress parameters, inflammasome activation, and pyroptosis markers. GLA demonstrated significant neuroprotective effects in SCI, as evidenced by improved locomotor recovery, attenuated tissue damage, and enhanced axonal regeneration in SCI model rats. Mechanistic studies revealed that GLA treatment potently activated the Nrf2/HO-1 signaling axis, leading to enhanced cellular antioxidant defenses and reduced reactive oxygen species accumulation in both in vivo and in vitro models. Concurrently, GLA effectively suppressed neuroinflammatory responses by inhibiting AIM2 inflammasome assembly, consequently reducing caspase-1 activation, gasdermin D-dependent pyroptosis, and interleukin-1β maturation in injured neurons. This study demonstrates that GLA exerts neuroprotective effects by activating the Nrf2/HO-1 antioxidant pathway and inhibiting AIM2 inflammasome-mediated pyroptosis. These findings suggest that GLA is a candidate drug with multi-target therapeutic potential, likely possessing clinical value for the treatment of SCI.
Indexed as
Identifiers
41699364What 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.