ArticleMolecular biology reports2026
Secoisolariciresinol diglucoside ameliorates muscarinic acetylcholine receptor mediated activation of NLRP3 inflammasome in cardiomyocytes.
Article in Molecular biology reports, 2026. 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSecoisolariciresinol diglucoside (SDG), the main lignan found in flaxseed, contributes to cardioprotection. However, its molecular mechanism of action remains unknown. NOD-like receptor protein containing domain 3 (NLRP3), a critical mediator in inflammatory pathways, is one of the key players in cardiovascular disease progression and is a promising target for cardioprotective interventions. This study investigated the immunomodulatory effect of SDG in regulating acetylcholine receptor-mediated activation of the NLRP3 inflammasome. METHODS AND
resultsHL-1 mouse cardiomyocytes were treated with carbachol, a cholinergic agonist, and analyzed for the expression and activation of NLRP3 family members (NLRP3, ASC, Caspase-1, IL-18, and IL-1beta). Investigations included preconditioning with SDG, NF-kappa B (NF-κB) inhibitor, or antagonists for acetylcholine receptors. NLRP3 components and NF-κB were analyzed by immunostaining and immunofluorescence. Caspase-1 activity and gasdermin D expression were studied as the functional endpoints of NLRP3 activation. Carbachol induced the activation of NLRP3 inflammasomes in HL-1 cardiomyocytes. Pre-treatment with SDG significantly attenuated the carbachol-induced activation of NLRP3 inflammasome. NLRP3 activation was also subdued in the presence of atropine, and NF-κB activation inhibitor, confirming the role of the muscarinic receptor and the NF-κB pathway, respectively.
conclusionThe study revealed the beneficial therapeutic properties of SDG as an anti-inflammatory agent that can help prevent NLRP3-induced inflammation. Further, the findings highlight the pro-inflammatory property of muscarinic cholinergic system, in contrast to the known nicotinic cholinergic anti-inflammatory system.
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.