In:
Journal of Biomedical Science, Springer Science and Business Media LLC, Vol. 18, No. 1 ( 2011-12)
Abstract:
Myocardial ischemia/reperfusion injury is the major cause of morbidity and mortality for cardiovascular diseases. Dopamine D 2 receptors are expressed in cardiac tissues. However, the roles of dopamine D 2 receptors in myocardial ischemia/reperfusion injury and cardiomyocyte apoptosis are unclear. Here we investigated the effects of both dopamine D 2 receptors agonist (bromocriptine) and antagonist (haloperidol) on apoptosis of cultured neonatal rat ventricular myocytes induced by ischemia/reperfusion injury. Methods Myocardial ischemia/reperfusion injury was simulated by incubating primarily cultured neonatal rat cardiomyocytes in ischemic (hypoxic) buffer solution for 2 h. Thereafter, these cells were incubated for 24 h in normal culture medium. Results Treatment of the cardiomyocytes with 10 μM bromocriptine significantly decreased lactate dehydrogenase activity, increased superoxide dismutase activity, and decreased malondialdehyde content in the culture medium. Bromocriptine significantly inhibited the release of cytochrome c , accumulation of [Ca 2+ ] i , and apoptosis induced by ischemia/reperfusion injury. Bromocriptine also down-regulated the expression of caspase-3 and -9, Fas and Fas ligand, and up-regulated Bcl-2 expression. In contrast, haloperidol (10 μM) had no significant effects on the apoptosis of cultured cardiomyocytes under the aforementioned conditions. Conclusions These data suggest that activation of dopamine D 2 receptors can inhibit apoptosis of cardiomyocytes encountered during ischemia/reperfusion damage through various pathways.
Type of Medium:
Online Resource
ISSN:
1423-0127
DOI:
10.1186/1423-0127-18-18
Language:
English
Publisher:
Springer Science and Business Media LLC
Publication Date:
2011
detail.hit.zdb_id:
1482918-6
