Effect of cerebrolysin on oxidative stress-induced apoptosis in an experimental rat model of myocardial ischemia.
Physiol Int
; 103(3): 310-320, 2016 Sep.
Article
en En
| MEDLINE
| ID: mdl-28229640
ABSTRACT
Apoptosis plays a role in the process of tissue damage after myocardial infarction (MI). This study was designed to investigate the possible effect of cerebrolysin against apoptosis triggered by oxidative cell stress in myocardial ischemia induced by isoproterenol in rat. Rats were pretreated with cerebrolysin 5 mL/kg intraperitoneally for 7 days and intoxicated with isoproterenol (ISO, 85 mg/kg, sc) on the last 2 days. Hearts were excised and stained to detect the infarction size. Serum levels of cardiotoxicity indices as creatine kinase isoenzyme (CK-MB) and troponin I (cTnI) as well as the cardiac oxidative stress parameters as thiobarbituric acid reactive substances and superoxide dismutase were estimated. The expression of prodeath gene p53 and antideath gene Bcl-2 was also assessed from the excised heart tissues. Leakage of cardiac enzymes, elevated oxidative stress markers, and apoptotic indices confirmed the MI occurring as a consequence of isoproterenol-induced ischemia. Cerebrolysin pretreatment caused significant attenuation of the oxidative stress-induced apoptosis in the ischemic myocardial tissue. These findings provided an evidence that cerebrolysin could protect rat myocardium against ischemic insult that was attributed to its antioxidant as well as its anti-apoptotic properties.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Isquemia Miocárdica
/
Estrés Oxidativo
/
Aminoácidos
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Physiol Int
Año:
2016
Tipo del documento:
Article
País de afiliación:
Egipto
Pais de publicación:
HU
/
HUNGARY
/
HUNGRIA