亚低温与缺血性神经元凋亡

Mild Hypothermia and Ischemic Neuronal Apoptosis

缺血性脑损伤后神经元凋亡的机制还不清楚 ,可能与内源性和外源性胱冬酶介导的细胞死亡途径的激活有关 ,但也可能与不依赖胱冬酶的凋亡诱导因子介导的凋亡有关。亚低温 (33～ 35℃ )可能是迄今惟一有效的神经保护措施 ,可以通过抑制胱冬酶活性、促进Bcl 2表达、影响神经元相关基因的表达等机制 ,减少脑缺血神经元凋亡 ,继而起到脑保护作用。

The mechanism of neuronal apoptosis after cerebral ischemic injury is poorly defined. It may be associated with the activation of the extrinsic and intrinsic pathways of caspase-mediated cell death, however, it may also be associated with the caspase-independent apoptosis-inducing factor (AIF) mediated apoptosis. Mild hypothermia (33-35℃) is possibly the only effective neuroprotective measure to date. Mild hypothermia may inhibit activity of caspases, promote Bcl-2 expression and affect neuron-related gene expression, and reduce neuronal apoptosis caused by cerebral ischemia and thus protect the brain.