摘要
目的:探讨强啡肽A1-13在新生鼠缺氧、缺血性脑损伤中作用的受体机制。方法:将7d龄新生鼠左侧颈总动脉结扎并在低氧环境下制成半球性脑缺氧、缺血模型,伤后即刻向小脑延髓池注射阿片κ受体拮抗剂nor-BNI或N-乙酰-D-门冬氨酸(NMDA)受体拮抗剂MK-801,比较其对损伤后脑含水量、脑内强啡肽A1-13免疫活性物质(ir-DynA1-13)、丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性的影响。结果:给予nor-BNI或MK-801均可降低损伤后的脑含水量,给药后皮层、海马ir-DynA1-13和/或MDA水平在脑损伤后的升高被部分逆转,SOD活性也部分恢复。MK-801恢复SOD活性的作用明显而nor-BNI的作用较弱。结论:强啡肽A1-13对新生鼠缺氧、缺血脑损伤的影响,很可能是通过阿片受体和NMDA受体途径共同作用而实现的,其影响的环节可能有所不同。
Objective:To explore the receptor mechanisms of dynorphinA 1-13 in hypoxic ischemic brain injury in neonatal rats.Method:Microinjection of either opioidκreceptor antagonist nor-BNI or N-methyl-D-aspartate(NMDA)receptor antagonist MK-801both at0.5mg/kg into the medulla pool was performed immediately after hypoxic ischemic brain injury of7d Sprague-Dawley rats prepared by a permanent ligation of left common carotid artery followed by a2.5h inhalation of humidified8%O 2 +92%N 2 at37℃.Effects of nor-BNI or MK-801on water content of the right and left hemispheres of the brain,levels of dynorphinA 1-13 immunoreactivity(ir-DynA1-13),malondialehyde(MDA)as well as the activity of superoxide dismutase(SOD)in cortex and hippocampus at different intervals following the damage were then investigated and statistically analyzed.Result:Microinjection of nor-BNI or MK-801might significantly decrease the water content of the brain and partially attenuate the magnitude of high levels of ir-DynA 1-13 and MDA and recuperate from the low activity of SOD due to brain damage.Activity of SOD was significantly recovered by MK-801rather than nor-BNI.Conclusion:Dynorphin may contribute to the pathophysiological changes of hypoxic ischemic brain injury via both opiate-receptor and NMDA-receptor mediated mechanisms with the possibility of different roles between the two.
出处
《中国康复医学杂志》
CAS
CSCD
2003年第6期345-347,共3页
Chinese Journal of Rehabilitation Medicine
基金
全军"九.五"医学科研规划科研基金资助(98D022)
