ArticleJournal of clinical biochemistry and nutrition2026
Micheliolide reduces the damage, pyroptosis and oxidative stress of cardiomyocytes caused by OGD/R by regulating the AMPK signaling pathway.
Article in Journal of clinical biochemistry and nutrition, 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
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.
- Micheliolide and ACT001 as Covalent Modulators of Inflammation-Redox-Metabolism Networks in CNS Disorders: An Evidence-Stratified Review of Mechanisms and Translational Challenges.Drug design, development and therapy · 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia-reperfusion (I/R) injury remains a devastating clinical problem, contributing substantially to morbidity and mortality worldwide. In the present study, we investigated the potential role of Micheliolide (MCL) in attenuating cardiac I/R injury. H9c2 cardiomyocytes were pretreated with MCL for 24 h and then subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). Cellular injury was evaluated by measuring cell viability and lactate dehydrogenase (LDH) release, while cell death was assessed using propidium iodide (PI) staining. Oxidative stress was determined by assessing superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, and glutathione peroxidase (GSH-Px) activity, while the expression levels of AMP-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC), and pyroptosis-related proteins were examined by Western blotting. The results demonstrated that MCL significantly alleviated OGD/R-induced damage in H9c2 cells. Moreover, MCL inhibited OGD/R-induced oxidative stress and pyroptosis while enhancing AMPK pathway activation. Importantly, the protective effect of MCL was attenuated in the presence of the AMPK inhibitor Compound C, indicating that activation of the AMPK signaling pathway is required for MCL-mediated cytoprotection.
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.