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目的 :探讨强啡肽A1-13 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A1-13 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A1-13 抗血清或nor-BM均可改善幼鼠伤后的一般状况 ,降低伤后 4 8h左侧脑含水量和乳酸含量 ,而以前者作用更为明显 ;强啡肽A1-13 抗血清可显著减轻皮层 ,海马细胞凋亡 ,nor -BMI此作用较弱。结论 :强啡肽A1-13 对新生鼠缺氧、缺血脑损伤的影响 ,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的。
Objective: To investigate the mechanism of dynorphin A1-13 in neonatal rats with hypoxic-ischemic brain damage. Methods: The left common carotid arteries of neonatal rats of 7d old age were ligated and hypoxic-ischemic brain damage model was made in hypoxia. Immediate injection of dynorphin A1-13 antisera or opioid kappa Body-antagonist nor-BNI at different times after administration compared the general status of young rats, brain water content, lactic acid content and apoptosis. Results: The dynorphin A1-13 antiserum or nor-BM can improve the general condition of the injured rats and reduce the content of the left brain water and the content of lactic acid 48 h after injury, Peptide A1-13 antiserum can significantly reduce apoptosis in cortex and hippocampus, and nor -MI has weak effect. CONCLUSION: The effect of dynorphin A1-13 on hypoxic and ischemic brain damage in newborn rats may not be through the opioid pathway, but may be achieved through other non-opioid pathways.