Key result
Intraperitoneal administration of the PKC inhibitor Ro-32-0432 reduced failure biomarkers, apoptosis, cardiac fibrosis, and pro-inflammatory cytokines in rats with experimental autoimmune myocarditis.
Why the study?
Does intraperitoneal administration of PKC inhibitor (Ro-32-0432) reduce failure biomarkers, apoptosis, fibrosis, and inflammation in Lewis rats with experimental autoimmune myocarditis?
Population
Lewis rats with experimental autoimmune myocarditis (EAM)
Design
Preclinical
Authors
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May support PKC inhibition in experimental myocarditis; leaves open translation to human disease.
Does intraperitoneal administration of PKC inhibitor (Ro-32-0432) reduce failure biomarkers, apoptosis, fibrosis, and inflammation in Lewis rats with experimental autoimmune myocarditis?
Inhibition of PKC with Ro-32-0432 reduces apoptosis, fibrosis, and inflammation in a rat model of experimental autoimmune myocarditis, suggesting a potential therapeutic strategy.
Zhong et al. (2017) studied Experimental autoimmune myocarditis. PKC inhibitor (Ro-32-0432) vs. Untreated EAM rats was evaluated on Expression of failure biomarkers, apoptosis, cardiac fibrosis, and pro-inflammatory cytokines. Intraperitoneal administration of the PKC inhibitor Ro-32-0432 reduced failure biomarkers, apoptosis, cardiac fibrosis, and pro-inflammatory cytokines in rats with experimental autoimmune myocarditis.
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