Effect of morphine preconditioning on neuronal apoptosis following cerebral ischemia/reperfusion injury

被引：3

作者：

Dong, He ^{[1
]}

Ji, Xiangyu ^{[1
]}

Wang, Dong ^{[1
]}

Ren, Yueyi ^{[2
]}

Wang, Shiduan ^{[1
]}

Song, Jianfang ^{[1
]}

机构：

[1] Qingdao Univ, Dept Anesthesiol, Affiliated Hosp, Qingdao 266003, Shandong, Peoples R China

[2] Women & Children Hlth Care Ctr Qingdao, Qingdao 266011, Shandong, Peoples R China

来源：

NEURAL REGENERATION RESEARCH | 2010年 / 5卷 / 15期

关键词：

morphine; brain ischemia; reperfusion; hippocampus; apoptosis; Caspase-3; rats; brain injury; neural regeneration; OPIOID RECEPTORS; TIME-COURSE; RAT-BRAIN; ISCHEMIA; DELTA; IMMUNOHISTOCHEMISTRY; NEUROPROTECTION; REPERFUSION; ACTIVATION; DEATH;

D O I：

10.3969/j.issn.1673-5374.2010.15.004

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Apoptosis, a form of neuronal damage, takes place following cerebral ischemia/reperfusion injury, and caspase-3 plays an important role in apoptosis. Studies have shown that morphine preconditioning influences neuronal apoptosis and related protein expression following cerebral ischemia/reperfusion injury. In the present study, neuronal degeneration was attenuated, and the number of apoptotic cells and caspase-3 expression decreased following morphine preconditioning in a rat model of cerebral ischemia/reperfusion injury. Moreover, pathological changes were attenuated with increasing morphine doses, as well as the number of apoptotic cells and caspase-3 expression. Results from the present study revealed that morphine preconditioning reduced ischemic brain injury and improved cerebral ischemic tolerance in a dose-dependent manner. The anti-apoptotic mechanism of morphine is closely related to Caspase-3.

引用

页码：1144 / 1149

页数：6

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