ArticleAnalytical cellular pathology (Amsterdam)2025
Sevoflurane Suppresses Cardiomyocyte Pyroptosis in Myocardial Ischemia via NLRP3 Inflammasome Signaling.
Article in Analytical cellular pathology (Amsterdam), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The purpose of this study was to investigate the impact of sevoflurane (SEV) on cardiomyocyte (CM) pyroptosis following myocardial ischemia (MI). Reverse validation was performed by pharmacologically activating NLRP3 with monosodium urate (MSU) to confirm that SEV's cardioprotective effects were specifically mediated through the NLRP3 inflammasome pathway. Sprague Dawley rats were randomly assigned to sham (sham), model (conventional anesthesia + MI-reperfusion [MIR] injury modeling), SEV (SEV inhalation anesthesia + MIR injury modeling), and SEV + NLRP3 (SEV inhalation anesthesia + MIR injury modeling + NLRP3) groups. The myocardial area at risk (MAAR) and the myocardial infarct size (MIS) were evaluated in each experimental group, and cardiac tissue was examined using hematoxylin-eosin (H&E), Masson trichrome, and TUNEL staining. The concentrations of creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), oxidative stress (OS), and pyroptosis-associated proteins and various inflammatory markers in the serum and cardiac tissue were quantified. Results showed that compared to the sham group, both model and SEV groups exhibited a significant increase in MAAR and MIS, accompanied by severe histopathological damage and noticeable OS (
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