Ontology highlight
ABSTRACT: Introduction
The molecular mechanisms underlying cardioprotection against doxorubicin (DOX)-induced myocardial injury are poorly understood. Histone deacetylase 2 (HDAC2) plays a significant role in oxidative stress, apoptosis, and mitochondrial dysfunction and is implicated in many human diseases, This study investigated the relationship between HDAC2 expression and DOX-induced myocardial injury using the in vivo rat model of DOX-induced cardiotoxicity and in vitro experiments with the H9c2 cardiomyocytes.Methods
The rat model of DOX-induced myocardial injury was established by administering DOX via intraperitoneal injections. HDAC2 expression was suppressed by administering rats with sodium butyrate (SB) via intraperitoneal injections. Echocardiography measu
SUBMITTER: Liu J
PROVIDER: S-EPMC11897267 | biostudies-literature | 2025
REPOSITORIES: biostudies-literature