促红细胞生成素可预防围产期窒息实验模型中缺氧/缺血诱导的DNA片段化。

Erythropoietin prevents hypoxia/ischemia-induced DNA fragmentation in an experimental model of perinatal asphyxia.

作者信息

Spandou Evangelia, Soubasi Vassiliki, Papoutsopoulou Stamatia, Karkavelas George, Simeonidou Constantina, Kaiki-Astara A, Guiba-Tziampiri Olympia

机构信息

Department of Physiology and Pharmacology, Faculty of Medicine, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece.

出版信息

Neurosci Lett. 2004 Aug 5;366(1):24-8. doi: 10.1016/j.neulet.2004.05.032.

DOI:10.1016/j.neulet.2004.05.032

PMID:15265583

Abstract

Erythropoietin (EPO) prevents neuronal damage following ischemic, metabolic and excitotoxic stress. Recent studies have shown that EPO plays a significant role in the developing brain. The present study investigates the effect of EPO administration on hypoxic-ischemic brain injury and the possibility that its neuroprotective action may be associated with anti-apoptotic activity. Seven-day-old rats were treated with EPO (2000 U/kg) and subjected to a modified Levine procedure. EPO administration before the hypoxic-ischemic insult significantly reduces the severity of brain damage and improved the short-term functional brain recovery. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling and DNA electrophoresis displayed no evidence of DNA fragmentation in EPO-treated animals. These results suggest that EPO might protect the neonatal rat brain by anti-apoptotic mechanisms.

摘要

促红细胞生成素（EPO）可预防缺血、代谢及兴奋性毒性应激后的神经元损伤。近期研究表明，EPO在发育中的大脑中发挥着重要作用。本研究探讨了给予EPO对缺氧缺血性脑损伤的影响，以及其神经保护作用可能与抗凋亡活性相关的可能性。对7日龄大鼠给予EPO（2000 U/kg）并采用改良的Levine法进行处理。在缺氧缺血性损伤前给予EPO可显著降低脑损伤严重程度，并改善脑功能的短期恢复。末端脱氧核苷酸转移酶介导的dUTP生物素缺口末端标记法及DNA电泳结果显示，接受EPO治疗的动物未出现DNA片段化迹象。这些结果表明，EPO可能通过抗凋亡机制保护新生大鼠脑。