ArticleResuscitation plus2025
Tubastatin A alleviates post-resuscitation myocardial damage possibly via inhibiting GSDME-mediated pyroptosis and MLKL-mediated necroptosis in a porcine model of cardiac arrest.
Article in Resuscitation plus, 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
Introduction: Global ischemia reperfusion (I/R) stimulation induced by cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) triggers multiple forms of programmed cell death including pyroptosis and necroptosis, and further results in post-resuscitation myocardial damage. Recently, a specific inhibitor of histone deacetylase 6 activity, tubastatin A (TubA) was preliminarily shown to protect the heart against global and regional I/R stimulation. The present study was designed to investigate the effect of TubA on post-resuscitation myocardial pyroptosis and necroptosis in a porcine model of CA and resuscitation. Methods: A total of 18 pigs were randomly assigned to one of the following three groups ( Results: After resuscitation, stroke volume and global ejection fraction were significantly decreased while serum cardiac troponin I and creatine kinase-MB were significantly increased in the two groups experiencing the CA/CPR procedure compared with the Sham group. However, myocardial dysfunction and cardiac injury were significantly milder in the CA/CPR + TubA group than in the CA/CPR group. At 24 h after resuscitation, apoptosis ratio, pyroptosis-related proteins (caspase 3, GSDME, GSDME-N), necroptosis-related proteins (RIP1, RIP3, MLKL, p-MLKL), and proinflammatory cytokines (high mobility group box 1, IL-1β, IL-18) in myocardium were significantly increased in the CA/CPR and CA/CPR + TubA groups compared with the Sham group. Nevertheless, all of them were significantly decreased in those pigs treated with the TubA compared to the CA/CPR group. Conclusions: TubA could effectively alleviate post-resuscitation myocardial damage in a porcine model of CA and resuscitation, in which the protective role was possibly related to the inhibition of GSDME-mediated pyroptosis and MLKL-mediated necroptosis.
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