CAJ | 학술논문

目的：探讨远端缺血后处理（RIPoC）在大鼠的全脑缺血再灌注（I/R）模型中的作用。方法采用四动脉阻断法（4-VO）将全脑I/R模型制作出来。将128只体重为200~250g的雄性SD大鼠随机分成两组，即I/R组和I/R+RIPoC组。在全脑缺血再灌注后七天取海马CA1区和额叶皮层组织进行Nissl染色，观察存活神经元密度；在全脑缺血再灌注后二十四小时和四十八小时采用TUNEL法对神经元凋亡进行检测；在全脑缺血再灌注后四天开始采用Morris水迷宫对空间学习和记忆能力的变化进行检测；在全脑缺血再灌注后四十八小时对超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和丙二醛（MDA）进行检测；在全脑缺血再灌注后二十四小时和四十八小时取海马CA1区组织采用Western blot及免疫组化法对凋亡相关蛋白Bcl-2、Bax的表达水平进行检测。结果和I/R组比较，I/R+RIPoC组中海马CA1区及额叶皮层中I/R后迟发性神经元死亡及TUNEL阳性细胞数量明显减少，两组间具有统计学差异（P<0.01）；空间学习和记忆能力的减退出现明显的改善，两组间具有统计学差异（P<0.05）；海马CA1区中Bcl-2明显上调，Bax明显下调，两组间具有统计学差异（P<0.01），SOD、CAT的活性明显增加，MDA水平明显降低，两组间具有统计学差异（P<0.01）。结论远端缺血后处理在大鼠的全脑缺血再灌注（I/R）模型中可以通过改善氧化应激水平，对凋亡相关蛋白进行调节，使大脑的迟发性神经元死亡得以减少，从而使空间学习与记忆能力得以改善，在全脑I/R损伤中起到保护神经的作用。
목적：탐토원단결혈후처리（RIPoC）재대서적전뇌결혈재관주（I/R）모형중적작용。방법채용사동맥조단법（4-VO）장전뇌I/R모형제작출래。장128지체중위200~250g적웅성SD대서수궤분성량조，즉I/R조화I/R+RIPoC조。재전뇌결혈재관주후칠천취해마CA1구화액협피층조직진행Nissl염색，관찰존활신경원밀도；재전뇌결혈재관주후이십사소시화사십팔소시채용TUNEL법대신경원조망진행검측；재전뇌결혈재관주후사천개시채용Morris수미궁대공간학습화기억능력적변화진행검측；재전뇌결혈재관주후사십팔소시대초양화물기화매（SOD）、과양화경매（CAT）화병이철（MDA）진행검측；재전뇌결혈재관주후이십사소시화사십팔소시취해마CA1구조직채용Western blot급면역조화법대조망상관단백Bcl-2、Bax적표체수평진행검측。결과화I/R조비교，I/R+RIPoC조중해마CA1구급액협피층중I/R후지발성신경원사망급TUNEL양성세포수량명현감소，량조간구유통계학차이（P<0.01）；공간학습화기억능력적감퇴출현명현적개선，량조간구유통계학차이（P<0.05）；해마CA1구중Bcl-2명현상조，Bax명현하조，량조간구유통계학차이（P<0.01），SOD、CAT적활성명현증가，MDA수평명현강저，량조간구유통계학차이（P<0.01）。결론원단결혈후처리재대서적전뇌결혈재관주（I/R）모형중가이통과개선양화응격수평，대조망상관단백진행조절，사대뇌적지발성신경원사망득이감소，종이사공간학습여기억능력득이개선，재전뇌I/R손상중기도보호신경적작용。
Objective: To investigate the effect of remote ischemic postconditioning (RIPoC) on rat cerebral ischemia reperfusion (I/R) model in rats. Methods:the four vessels occlusion method (4-VO) will be made with the whole brain I/R model. 128 the weight of 200-250gmale SD rats were randomly divided into two groups, namely I/R group and I/R+RIPoC group. Seven days later, after cerebral ischemic reperfusion in hippocampal CA1 region and the frontal cortex tissues were stained with Nissl and observed in the survival neurondensity. in the global cerebral ischemia/reperfusion after twenty-four hours and forty-eight hours of using TUNEL to detect the apoptosis of neurons in cerebral ischemia reperfusion;four days after the Morris water maze was used to change the the ability of spatial learning and memory were detected;in the forty-eight hours after cerebral ischemia and reperfusionon superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) were detected; in the global cerebral ischemia / reperfusion after twenty-four hours and forty-eight hours in CA1 area of hippocampus tissue by Western blot and immunohistochemistrymethod the expression level of apoptosis related protein Bcl-2, Bax were detected. Results:compared with group I/R, group I/R+RIPoC in CA1 region of hippocampus and prefrontal cortex in I/R delayed neuronal death and the number of TUNEL positive cells was signiifcantly reduced, with statistical difference between the two groups (P<0.01); spatial learning and memory ability decreased significantly improved, with statistical differencebetween the two groups (P<0.05);hippocampus CA1 Bcl-2 was signiifcantly increased, Baxdecreased, with signiifcant difference between the two groups (P<0.01), SOD, CAT activity was signiifcantly increased, MDA levels were signiifcantly lower, with signiifcant difference between the two groups (P<0.01). Conclusion the distal ischemic postconditioning in ratswith cerebral ischemia reperfusion (I/R) model can improve the level of oxidative stress, apoptosis related protein to regulate the brain. The delayed neuronal death can be reduced so that the spatial learning and memory ability can be improved. Thus it plays a protective effect of the nerve of during the injury of cerebral I/R.