Key result
PRCP overexpression reverses myocardial ischemia-reperfusion injury in rats.
Why the study?
The mechanism and cardiac protective effects of prolylcarboxypeptidase against myocardial ischemia-reperfusion injury were not fully understood.
Does PRCP overexpression protect against myocardial ischemia-reperfusion injury in male SD rats?
RCT (n=36)
randomly divided
Does PRCP overexpression protect against myocardial ischemia-reperfusion injury in male SD rats?
p-value: p=< 0.05
PRCP overexpression protects against myocardial ischemia-reperfusion injury in rats by inhibiting NLRP3-mediated cell pyroptosis.
May protect against myocardial ischemia-reperfusion injury; leaves open translation from rodent models to clinical practice.
Objective To investigate the way in which prolylcarboxypeptidase (PRCP) protects against myocardial ischemia-reperfusion injury (MIRI) and the mechanisms that underlie it. Method A surgical ligation of the coronary artery was adopted to establish a myocardial ischemia-reperfusion model in male SD rats. Thirty-six rats were randomly divided into six groups: Normal group, Sham group, MIRI model group, empty vector (MIRI + EZ.null) group, PRCP overexpression (MIRI + PRCP) group, and nicorandil (MIRI + Nic) group, with 6 rats in each group. The rats received an injection of PRCP's adeno-associated virus 9 (AAV9) through the tail vein 3 weeks prior to the modeling. Results Compared with the Normal and Sham groups, the expression levels of NOD-like receptor thermal protein domain-associated protein 3 (NLRP3), Caspase-1, IL-18, IL-1β, and GSDMD in the MIRI group and MIRI + EZ-null group were significantly increased ( P < 0.05). Myocardial apoptosis index, myocardial infarction size, ejection fraction, and short axis shortening rate were significantly increased ( P < 0.05). At the same time, PRCP and nicorandil therapy could reverse the damage effect caused by MIRI ( P < 0.05). Conclusion PRCP can lessen MIRI and protect cardiac function in rats by inhibiting NLRP3/Capase-1/IL-18/IL-1β signaling pathway-mediated cell pyroptosis.
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He et al. (2025) conducted an RCT in myocardial ischemia-reperfusion injury (MIRI) (n=36). prolylcarboxypeptidase (PRCP) overexpression vs. MIRI model group and empty vector group was evaluated on expression levels of NLRP3, Caspase-1, IL-18, IL-1β, GSDMD, myocardial apoptosis index, myocardial infarction size, ejection fraction, and short axis shortening rate (p=< 0.05). PRCP overexpression significantly reversed the damage effect caused by myocardial ischemia-reperfusion injury in rats (P < 0.05).
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