Elsayed M H, Hogan T P, Shaw P L, Castro A J
Department of Pediatrics, Loyola University Medical Center, Maywood, Illinois 60153, USA.
Exp Neurol. 1996 Jan;137(1):127-41. doi: 10.1006/exnr.1996.0013.
In view of numerous studies demonstrating that intracerebral implants of fetal neural tissue can promote functional recovery and structural repair in the damaged brain, the present study examined the potential use of neocortical transplantation in newborn rats that sustained hypoxic-ischemic brain injury. Ischemic insult was induced in Long-Evans, black-hooded 1-week-old rats by unilateral common carotid artery occlusion followed by 2.5 h of hypoxia in 8% O2. One week later, animals received neocortical block transplants. At 2-6 weeks posttransplantation, animals were sacrificed and their brains examined histologically. Transplants survived in over 80% of the animals and the presence of acetylcholinesterase-positive fibers crossing the host-transplant interface provided evidence of transplant integration with the host brain. However, morphometric measurements revealed that the transplants were unable to reduce the hypoxia-ischemia-induced degeneration in the host hippocampus, caudate-putamen, or thalamus. Nonetheless the demonstrated survival of grafts in the neonatal hypoxia-ischemia model suggests a potential therapeutic effect.
鉴于大量研究表明，向脑内植入胎儿神经组织可促进受损大脑的功能恢复和结构修复，本研究检测了新皮质移植在遭受缺氧缺血性脑损伤的新生大鼠中的潜在应用。通过单侧颈总动脉闭塞，然后在8%氧气环境中缺氧2.5小时，在1周龄的Long-Evans黑帽大鼠中诱导缺血性损伤。1周后，动物接受新皮质块移植。移植后2至6周，处死动物并对其大脑进行组织学检查。超过80%的动物移植组织存活，并且存在穿过宿主-移植界面的乙酰胆碱酯酶阳性纤维，这为移植组织与宿主脑整合提供了证据。然而，形态学测量显示，移植组织无法减轻缺氧缺血诱导的宿主海马体、尾状核-壳核或丘脑的变性。尽管如此，在新生缺氧缺血模型中移植组织的存活证明了其潜在的治疗作用。
