Department of Neurology, the First Clinical Medical College of Harbin Medical University, Harbin 150001, China.
Brain Res. 2011 Jan 12;1368:59-64. doi: 10.1016/j.brainres.2010.10.073. Epub 2010 Oct 25.
In addition to pharmacological treatment of ischemic stroke, hypothermia has been proposed to be a therapeutic option for protecting brain cells from ischemic death. Less is known about the molecular mechanisms underlying this hypothermic protection of ischemic cells, which we have investigated in rats. In four groups of experiments, ischemia under the conditions of normothermia and mild hypothermia as well as sham-operation under these two conditions, we have analyzed quantitatively the score of neurological impairment and the expression of second mitochondrion -derived activator of caspases (SMAC), an index of cellular apoptosis. Compared with ischemia under normothermia, the treatment of mild hypothermia significantly improves brain function and lowers SMAC expression. Our results indicate that the mild hypothermia protects the functions of brain cells from ischemic impairment through attenuating apoptotic death.
除了对缺血性中风进行药物治疗外，还提出低温治疗是保护脑细胞免受缺血性死亡的一种治疗选择。对于低温保护缺血细胞的分子机制，人们知之甚少，我们在大鼠中对此进行了研究。在四组实验中，我们在常温及轻度低温条件下进行了缺血，以及在这两种条件下进行了假手术，定量分析了神经损伤评分和第二线粒体衍生的半胱天冬酶激活剂（SMAC）的表达，SMAC 是细胞凋亡的一个指标。与常温下的缺血相比，轻度低温治疗显著改善了大脑功能并降低了 SMAC 的表达。我们的结果表明，轻度低温通过减轻细胞凋亡死亡来保护脑细胞的功能免受缺血损伤。
