Neuroprotective Effects of Activated Protein C Through Induction of Insulin-Like Growth Factor-1 (IGF-1), IGF-1 Receptor, and Its Downstream Signal Phosphorylated Serine-Threonine Kinase After Spinal Cord Ischemia in Rabbits
Neuroprotective Effects of Activated Protein C Through Induction of Insulin-Like Growth Factor-1 (IGF-1), IGF-1 Receptor, and Its Downstream Signal Phosphorylated Serine-Threonine Kinase After Spinal Cord Ischemia in Rabbits
复制标题
兔脊髓缺血后活化蛋白 C 通过诱导胰岛素样生长因子-1 (IGF-1)、IGF-1 受体及其下游信号磷酸化丝氨酸-苏氨酸激酶的神经保护作用
作者：
Takashi Yamauchi;M. Sakurai;K. Abe;H. Takano;Y. Sawa
背景与目的活化蛋白C （Activated protein C， APC）在神经元缺血再灌注损伤中具有有益作用。然而，这种有益作用的可能机制尚不完全清楚。本研究旨在探讨APC对缺血性脊髓损伤的影响及其可能的机制。方法：在脊髓缺血诱导后，静脉注射APC （A组）或载药（I组）。通过计数运动神经元的数量来分析缺血损伤的严重程度。为了研究APC预防缺血性脊髓损伤的机制，我们对胰岛素样生长因子1 （IGF-1）、IGF-1受体和磷酸化丝氨酸-苏氨酸激酶（p-Akt）进行免疫反应性和Western blot检测。结果- APC减轻了缺血后运动神经元的功能缺陷，增加了运动神经元的数量。再灌注后8 h， A组IGF-1的免疫反应性较I组强，但1 d时与I组相同。a组对IGF-1受体和下游因子p-Akt的诱导作用更强，持续时间更长。结论-这些结果表明，IGF-1、IGF-1受体和p-Akt的诱导可能部分解释了APC在兔短暂性脊髓缺血后的神经保护作用。
Background and Purpose— Activated protein C (APC) has beneficial effects on ischemia reperfusion injury in neuron. However, the possible mechanism of such beneficial effects is not fully understood. The aim of this study was to investigate the effects and possible mechanisms of APC on ischemic spinal cord damage. Methods— After induction of spinal cord ischemia, APC (group A) or vehicle (group I) was injected intravenously. Severity of ischemic damage was analyzed by counting the number of motor neurons. To investigate the mechanisms by which APC prevents ischemic spinal cord damage, we performed immunoreactivity and Western blotting of insulin-like growth factor 1 (IGF-1), IGF-1 receptor, and phosphorylated serine-threonine kinase (p-Akt). Results— APC eased the functional deficits and increased the number of motor neurons after ischemia. Immunoreactivity of IGF-1 in group A was stronger than in group I at 8 hours after reperfusion but was at the same level at 1 day. Induction of IGF-1 receptor and the downstream factor p-Akt was stronger and more prolonged in group A. Conclusions— These results indicate that induction of IGF-1, IGF-1 receptor, and p-Akt might partially explain the neuroprotective effects of APC after transient spinal cord ischemia in rabbit.
影响因子：
15.9
作者：
Li, Q;Li, BS;Anversa, P
通讯作者：
Anversa, P