Association of Parkinson Disease Induction with Cardiac Upregulation of Apoptotic Mediators P53 and Active Caspase-3: An Immunohistochemistry Study.

Abstract

BackgroundApoptosis plays a key role in the pathogenesis of Parkinson disease (PD). Active caspase-3, which is a proapoptotic factor, has been shown to reduce cardiac contractility, causing cardiac dysfunction in many pathological diseases. Reduced cardiac contractility and cardiac autonomic dysfunction have been reported in PD patients and PD mice treated with MPTP. The aim of this study was to show the impact of PD induction on the expression of the apoptotic mediators p53 and active caspase-3 in the heart.Material/MethodsEqual control and PD groups were formed by 20 randomly selected normal albino mice. We used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (25 mg/kg) and probenecid (250 mg/kg) (MPTP/p) to induce chronic Parkinsonism in the PD group. Immunohistochemistry was performed to investigate the expression of p53, active caspase-3, and β-adrenergic receptor in hearts from the 2 animal groups.ResultsP53 and active caspase-3 expression was significantly higher in PD hearts than in the control hearts (p value <0.01). β-adrenergic receptor expression was significantly lower in PD hearts than in control hearts (p value <0.01).ConclusionsOur results show an association of PD with p53 and active caspase-3 overexpression and β-adrenergic receptor underexpression in the heart, potentially promoting the cardiac autonomic dysfunction frequently observed in PD.