摘要
目的:探讨强啡肽A_(1-13)在新生鼠缺氧缺血性脑损伤中的作用机制。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缺氧缺血性脑损伤模型,伤后即刻向小脑延髓池注射强啡肽A_(1-13)抗血清或阿片κ受体拮抗剂nor-BNI,给药后不同时间比较其对幼鼠一般状况、脑含水量、乳酸含量和细胞凋亡的影响。结果:给予强啡肽A_(1-13)抗血清或nor—BNI均可改善幼鼠伤后的一般状况,降低伤后48h左侧脑含水量和乳酸含量,而以前者作用更为明显;强啡肽抗A_(1-13)血清可显著减轻皮层、海马细胞调亡,nor-BNI此作用较弱。结论:强啡肽A_(1-13)对新生鼠缺氧缺血性脑损伤的影响,除通过阿片途径外,尚可能通过其它非阿片途径共同作用而实现。
Objective: To explore the mechanisms of dynorphin A_(1-13) in hypoxic ischemic brain injury in neonatal rata. Methods: Microinjection of either anti-dynorphin A_(1-13) serum(5/11) or opioid k receptor antagonist nor-binaltorphimine(nor-BNI, 1.5μg for each)into the medulla pool was performed immediately after hypoxic ischemic brain injury of 7d SD rata prepared by a permanent ligafion of left common carotid artery followed by a 2.5 h inhalation of humidified 8% O_2+92 N_2 at 37℃. Effect of anti-dynorphin A_(1-13) serum or nor-BNI on general conditions of pups 3, 10, 15rain postadministration, water content of the brain, cell apoptosis and changes of level of lactic acid 24 h post-administion were thenin vestigated and statistically analyzed. Results: Microinjection of both anti-dynorphin A_(1-13) serum and nor-BNI might significandy improve pup general conditions, alleviate brain edema, decrease the high level of lactic acid resulted from the brain injury with more significant effect of anti-dynorphin A_+(1-13) serum than of nor-BNI. Attenuation of the great magnitude of cell apoptosis was obvious by anti-dynrophin A_(1-13) serum rather than by nor-BNI. Conclusion: Present data suggest that dynorphin A_(1-13) contributes to the pathophysiological changes of hypoxic ischemic brain injury not only via opioidreceptor mediation but probably a combination of nonopioid mechanisms.
出处
《福州总医院学报》
2002年第2期96-99,共4页
Journal of Fuzhou General Hospital
