ArticleHistology and histopathology2026
Tanshinone IIA alleviates inflammation and apoptosis in myocardial ischemia-reperfusion injury by modulating the MALT1/NF-κB/NLRP3 signaling axis.
Article in Histology and histopathology, 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
10 authors.
Funding
Abstract
objectiveTanshinone IIA (Tan IIA), a bioactive compound from
methodsWe established a myocardial I/R injury model in rats by coronary artery ligation and created a hypoxia/reoxygenation (H/R) cell model for experimental investigation. The expression levels of relevant genes and proteins were assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot. Cellular viability and myocardial tissue damage were evaluated through cell counting kit-8 (CCK-8) assay, biochemical test kits, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, hematoxylin-eosin (HE) staining, and triphenyltetrazolium chloride (TTC) staining.
resultsThis study demonstrated that Tan IIA treatment significantly reduced serum levels of cardiac troponin T (cTnT), creatine kinase-MB (CK-MB), and lactate dehydrogenase (LDH) in rats with myocardial I/R injury. It also suppressed the expression of inflammatory factors-tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-18, and IL-6-in myocardial tissue, inhibited apoptosis, diminished myocardial infarct size, and ultimately ameliorated histopathological damage. Meanwhile, in H9C2 cells subjected to H/R injury, Tan IIA treatment enhanced cell viability and attenuated inflammatory response and apoptosis. Mechanistically, Tan IIA downregulated mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1), leading to suppressed expression and nuclear translocation of nuclear factor kappa B (NF-κB), which subsequently inhibited the activation of the NOD-like receptor thermal protein domain-associated protein 3 (NLRP3). This cascade alleviated I/R-induced myocardial inflammation and apoptosis, thereby conferring protection against myocardial I/R injury.
conclusionTan IIA attenuated I/R-induced myocardial inflammation and apoptosis through the inhibition of the MALT1/NF-κB/NLRP3 signaling pathway, ultimately alleviating myocardial I/R injury.
Indexed as
Identifiers
41978498What 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.