CAJ | 학술논문

[目的] 探讨丝裂原活化蛋白激酶家族(MAPK)在Swedish 突变的淀粉样前体蛋白(APP/SWE)转基因鼠脑缺血中的作用.[方法] APP/SWE 转基因鼠与非转基因鼠各12 只应用光化学法诱导脑梗塞形成,缺血7 d后其中6只以尼氏染色对缺血半暗带区存活神经元进行定量分析,6只以Western blot方法检测p38MAPK和JNK的活性. [结果] 缺血7 d后,非转基因鼠组缺血半球海马区缺血半暗带存活神经元数目与非缺血半球镜像部位神经元数目的比值(78.3 ± 1.3)%与APP/SWE转基因鼠组(70.5 ± 1.4)%有统计学差异(P ＜ 0.05);APP/SWE转基因鼠组缺血半球p38MAPK和JNK活性与非缺血半球有统计学差异(P ＜ 0.05),而非转基因鼠组缺血半球p38MAPK和JNK活性与非缺血半球差异无统计学意义(P ＞ 0.05).[结论] APP/SWE转基因鼠组缺血后脑损伤显著重于非转基因鼠组,可能的机制与丝裂原活化蛋白激酶过度激活促进脑缺血后细胞凋亡过程有关.
[목적] 탐토사렬원활화단백격매가족(MAPK)재Swedish 돌변적정분양전체단백(APP/SWE)전기인서뇌결혈중적작용.[방법] APP/SWE 전기인서여비전기인서각12 지응용광화학법유도뇌경새형성,결혈7 d후기중6지이니씨염색대결혈반암대구존활신경원진행정량분석,6지이Western blot방법검측p38MAPK화JNK적활성. [결과] 결혈7 d후,비전기인서조결혈반구해마구결혈반암대존활신경원수목여비결혈반구경상부위신경원수목적비치(78.3 ± 1.3)%여APP/SWE전기인서조(70.5 ± 1.4)%유통계학차이(P ＜ 0.05);APP/SWE전기인서조결혈반구p38MAPK화JNK활성여비결혈반구유통계학차이(P ＜ 0.05),이비전기인서조결혈반구p38MAPK화JNK활성여비결혈반구차이무통계학의의(P ＞ 0.05).[결론] APP/SWE전기인서조결혈후뇌손상현저중우비전기인서조,가능적궤제여사렬원활화단백격매과도격활촉진뇌결혈후세포조망과정유관.
[Objective] To investigate the effect of mitogen-activated protein kinases (MAPK) on cerebral ischemia induced by photothrombosis in Swedish amyloid precursor protein (APP/SWE) transgenic mice.[Methods] In APP/SWE transgenic mice and non-transgenic mice (n ＝ 12,respectively),photothrombotic stroke was induced,on 7 d after cerebral ischemia,the amount of the survival neuron in the penumbra was counted using Nissl staining (n ＝ 6),and the activities of p38MAPK and JNK were measured by Western blot (n ＝ 6).[Results] On 7 d after cerebral ischemia,ratio of amount of survival neuron over the penumbra in hippocampus in the ischemic side to that in the non-ischemic side in the non-transgenic mice group (78.3 ± 1.3)% was significantly higher than that in the APP/SWE transgenic mice group (70.5 ± 1.4)% (P ＜ 0.05);compared with the non-ischemic hemisphere,the activities of p38 MAPK and JNK increased significantly in the ischemic hemisphere in the APP/SWE transgenic mice group (P ＜ 0.05),whereas,there was no significant difference between ischemic and non-ischemic hemisphere in the non-transgenic mice group (P ＞ 0.05).[Conclusion] Photothrombosis causes more severe damage in the APP/SWE transgenic mice group than that in the non-transgenic mice group.The possible mechanism includes the increased activities of MAPK which enhance the process of neuronal cell apoptosis.