摘要
p53是重要的肿瘤抑制因子,在细胞内起着抑制细胞周期、促进基因组修复和诱导凋亡等多重作用。在蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后,p53在缺氧等多种因素作用下被激活,并通过其靶蛋白、Bcl-2和Caspase家族蛋白等发挥促血管内皮细胞及脑内神经元凋亡的作用,并导致SAH后早期脑损伤和后期血管痉挛的发生。应用p53特异性的抑制剂可以阻断p53的活化,显著恢复SAH后的血脑屏障功能并缓解脑血管痉挛。本文讨论了p53在SAH后的血管内皮细胞和神经元凋亡中的作用机制,并进一步探讨应用p53抑制剂拮抗p53功能以治疗SAH后早期脑损伤和血管痉挛的可能性。
p53 is an important tumor suppressor, which can arrest the cell cycle, repair the damaged genes and lead to massive apoptosis. After subarachnoid hemorrhage（SAH）,p53 is activated by some stress factors（such as hypoxia） and play the roles in the apoptosis of endothelial ceils and neurons through modulation its target protein,Bcl-2 proteins and activation of caspase proteins. The apoptosis mentioned above can lead to the early brain injury and vasospasm after SAH. Furthermore, the treatment of p53 inhibitor （such as pifithrin- eL ）can block the activation of p53, consequently restore the blood-brain barrier integrity and result in complete attenuation of vasospasm. Here, we will discuss the mechanism of p53 in the apoptosis of endothelial cells and neurons after SAH and probe the possibility of p53 inhibitor in the prevention of the early brain injury and vasospasm.
出处
《解剖科学进展》
CAS
2009年第2期227-232,共6页
Progress of Anatomical Sciences
基金
国家自然科学基金资助项目(30672157)
