- 作者: Hong-zhu Li; Jin Guo; Jun Gao; Li-ping Han; Chun-ming Jiang; Hong-xia Li; Shu-zhi Bai Bai; Wei-hua Zhang; Guang-wei Li; Li-na Wang; Hong Li; Ya-jun Zhao; Yan Lin; Ye Tian; Guang-dong Yang; Rui Wang; Ling-yun Wu; Bao-feng Yang; Chang-qing Xu
- 作者服務機構: Department of Pathophysiology, Harbin Medical University, Harbin, Mainland China
- 中文摘要: --
- 英文摘要:
Background: Myocardial ischemia/reperfusion injury is the major cause of morbidity
and mortality for cardiovascular diseases. Dopamine D2 receptors are expressed in
cardiac tissues. However, the roles of dopamine D2 receptors in myocardial
ischemia/reperfusion injury and cardiomyocyte apoptosis are unclear. Here we
investigated the effects of both dopamine D2 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 2h. Thereafter, these cells were incubated for 24h 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 [Ca2+]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 D2 receptors can inhibit
apoptosis of cardiomyocytes encountered during ischemia/reperfusion damage
through various pathways. - 中文關鍵字: --
- 英文關鍵字: --