CAJ | 학술논문

目的：研究内源性组胺在前脑缺血再灌注后期的神经保护作用。方法：将野生型（ WT ）小鼠和组氨酸脱羧酶基因敲除（ HDC-KO）小鼠各随机分为对照组和缺血组，缺血组小鼠双侧颈总动脉夹闭30 min以建立前脑缺血模型，比较再灌后WT和HDC-KO小鼠的体重变化和死亡率，并在再灌14 d时对各组存活小鼠进行条件性恐惧学习记忆测试，再灌3 d及15 d时，对各组小鼠取脑，制作冰冻切片，进行甲苯胺蓝染色，观察海马CA1区神经元损伤情况。结果：再灌1 d后，WT和HDC-KO小鼠均出现体重下降，再灌4 d、5 d、6 d及7 d后，HDC-KO小鼠的体重恢复程度均显著低于WT小鼠。前脑缺血再灌8～14 d，HDC-KO小鼠的死亡率显著高于WT小鼠（ P＜0.05）。再灌14 d后，HDC-KO小鼠的背景及线索记忆能力均显著低于WT小鼠（ P＜0.05）。再灌3 d后，HDC-KO和WT小鼠的海马CA1区神经元密度无显著差异，而再灌15 d后，HDC-KO小鼠海马CA1区神经元密度显著低于WT小鼠（ P＜0.05）。结论：内源性组胺可减轻脑缺血再灌注后期的学习记忆能力下降及神经元缺失，但其作用机制有待进一步研究。
목적：연구내원성조알재전뇌결혈재관주후기적신경보호작용。방법：장야생형（ WT ）소서화조안산탈최매기인고제（ HDC-KO）소서각수궤분위대조조화결혈조，결혈조소서쌍측경총동맥협폐30 min이건립전뇌결혈모형，비교재관후WT화HDC-KO소서적체중변화화사망솔，병재재관14 d시대각조존활소서진행조건성공구학습기억측시，재관3 d급15 d시，대각조소서취뇌，제작빙동절편，진행갑분알람염색，관찰해마CA1구신경원손상정황。결과：재관1 d후，WT화HDC-KO소서균출현체중하강，재관4 d、5 d、6 d급7 d후，HDC-KO소서적체중회복정도균현저저우WT소서。전뇌결혈재관8～14 d，HDC-KO소서적사망솔현저고우WT소서（ P＜0.05）。재관14 d후，HDC-KO소서적배경급선색기억능력균현저저우WT소서（ P＜0.05）。재관3 d후，HDC-KO화WT소서적해마CA1구신경원밀도무현저차이，이재관15 d후，HDC-KO소서해마CA1구신경원밀도현저저우WT소서（ P＜0.05）。결론：내원성조알가감경뇌결혈재관주후기적학습기억능력하강급신경원결실，단기작용궤제유대진일보연구。
AIM: To determine the effect of endogenous histamine on transient forebrain ischemia-induced neuronal injury at the late phase of reperfusion using histidine decarboxylase knockout ( HDC-KO) mice.METHODS:Wild-type (WT) and HDC-KO mice were subjected to bilateral common carotid artery occlusion for 30 min followed by 3 d or 15 d of reperfusion.At different time points after reperfusion, the body weight, mortality rate, learning and memory in fear conditioning test and hippocampal CA 1 neuronal density were evaluated .RESULTS: At 1 d after reperfusion , the body weight loss was observed in both WT and HDC-KO mice.At 4 d, 5 d, 6 d and 7 d after reperfusion, the increment in the body weight of the HDC-KO mice was significantly smaller than that of the WT mice .During the period between 8 d and 14 d after reperfusion, the mortality rate of the HDC-KO mice was higher than that of the WT mice (P<0.05).At 14 d after reperfusion , the HDC-KO mice exhibited more aggravated deficits in contextual and cue memory compared with the WT mice.Correspondingly , a more severe CA1 neuronal injury in the HDC-KO mice than that in the WT mice was ob-served at 15 d but not at 3 d after reperfusion (P<0.05).CONCLUSION:Endogenous histamine may attenuate learn-ing/memory deficits and neuronal injury at the late phase of ischemia /reperfusion.However, the involved mechanisms need to be further investigated .