国际脑血管病杂志
國際腦血管病雜誌
국제뇌혈관병잡지
INTERNATIONAL JOURNAL OF CEREBROVASCULAR DISEASES
2015年
3期
189-192
,共4页
补娟%牛晓珊%党辉%马毓%沙晶%景燕%艾山江%朱沂%王展波
補娟%牛曉珊%黨輝%馬毓%沙晶%景燕%艾山江%硃沂%王展波
보연%우효산%당휘%마육%사정%경연%애산강%주기%왕전파
脑缺血%再灌注损伤%AMP-活化蛋白激酶%细胞色素c组%疾病模型,动物%小鼠
腦缺血%再灌註損傷%AMP-活化蛋白激酶%細胞色素c組%疾病模型,動物%小鼠
뇌결혈%재관주손상%AMP-활화단백격매%세포색소c조%질병모형,동물%소서
Brain Ischemia%Reperfusion Injury%AMP-Activated Protein Kinases%Cytochrome c Group%Disease Models,Animal%Mice
目的:研究抑制 AMP 活化的蛋白激酶(AMP-activated protein kinase, AMPK)活性对小鼠脑缺血再灌注后皮质和海马细胞色素 c(cytochrome c, CytC)的影响。方法36只雄性 C57BL/6小鼠,采用随机数字法分为假手术组、缺血再灌注组和 compound C 组,每组12只。 compound C 组在缺血时腹腔注射 AMPK 特异性抑制剂 compound C(20 mg/kg)。采用改良线栓法制作大脑中动脉闭塞模型,再灌注24 h后采用蛋白印迹法测定缺血侧皮质和海马 AMPK、磷酸化 AMPA(phosphorylated-AMPK, p-AMPK)和细胞质 CytC 表达水平。结果假手术组、缺血再灌注组和 compound C 组皮质 p-AMPK/AMPK 分别为0.701±0.197、1.408±0.322和0.930±0.229(F =12.000,P =0.001),海马分别为0.685±0.228、1.507±0.418和0.964±0.378( F =8.530,P =0.003),缺血再灌注组皮质( P <0.001)和海马(P =0.001)均显著高于假手术组,compound C 组皮质(P =0.005)和海马(P =0.017)均显著低于缺血再灌注组。假手术组、缺血再灌注组和 compound C 组皮质 CytC 水平分别为0.496±0.278、1.461±0.321和1.018±0.175( F =19.915,P <0.001),海马分别为0.511±0.257、1.610±0.441和0.921±0.228(F =17.795,P <0.001),缺血再灌注组皮质(P <0.001)和海马(P <0.001) CytC 水平均显著高于假手术组,而 compound C 组皮质(P =0.011)和海马(P =0.002)细胞质 CytC水平均显著低于脑缺血再灌注组。结论抑制 AMPK 活性能下调小鼠脑缺血再灌注后缺血侧皮质和海马细胞质 CytC 表达。
目的:研究抑製 AMP 活化的蛋白激酶(AMP-activated protein kinase, AMPK)活性對小鼠腦缺血再灌註後皮質和海馬細胞色素 c(cytochrome c, CytC)的影響。方法36隻雄性 C57BL/6小鼠,採用隨機數字法分為假手術組、缺血再灌註組和 compound C 組,每組12隻。 compound C 組在缺血時腹腔註射 AMPK 特異性抑製劑 compound C(20 mg/kg)。採用改良線栓法製作大腦中動脈閉塞模型,再灌註24 h後採用蛋白印跡法測定缺血側皮質和海馬 AMPK、燐痠化 AMPA(phosphorylated-AMPK, p-AMPK)和細胞質 CytC 錶達水平。結果假手術組、缺血再灌註組和 compound C 組皮質 p-AMPK/AMPK 分彆為0.701±0.197、1.408±0.322和0.930±0.229(F =12.000,P =0.001),海馬分彆為0.685±0.228、1.507±0.418和0.964±0.378( F =8.530,P =0.003),缺血再灌註組皮質( P <0.001)和海馬(P =0.001)均顯著高于假手術組,compound C 組皮質(P =0.005)和海馬(P =0.017)均顯著低于缺血再灌註組。假手術組、缺血再灌註組和 compound C 組皮質 CytC 水平分彆為0.496±0.278、1.461±0.321和1.018±0.175( F =19.915,P <0.001),海馬分彆為0.511±0.257、1.610±0.441和0.921±0.228(F =17.795,P <0.001),缺血再灌註組皮質(P <0.001)和海馬(P <0.001) CytC 水平均顯著高于假手術組,而 compound C 組皮質(P =0.011)和海馬(P =0.002)細胞質 CytC水平均顯著低于腦缺血再灌註組。結論抑製 AMPK 活性能下調小鼠腦缺血再灌註後缺血側皮質和海馬細胞質 CytC 錶達。
목적:연구억제 AMP 활화적단백격매(AMP-activated protein kinase, AMPK)활성대소서뇌결혈재관주후피질화해마세포색소 c(cytochrome c, CytC)적영향。방법36지웅성 C57BL/6소서,채용수궤수자법분위가수술조、결혈재관주조화 compound C 조,매조12지。 compound C 조재결혈시복강주사 AMPK 특이성억제제 compound C(20 mg/kg)。채용개량선전법제작대뇌중동맥폐새모형,재관주24 h후채용단백인적법측정결혈측피질화해마 AMPK、린산화 AMPA(phosphorylated-AMPK, p-AMPK)화세포질 CytC 표체수평。결과가수술조、결혈재관주조화 compound C 조피질 p-AMPK/AMPK 분별위0.701±0.197、1.408±0.322화0.930±0.229(F =12.000,P =0.001),해마분별위0.685±0.228、1.507±0.418화0.964±0.378( F =8.530,P =0.003),결혈재관주조피질( P <0.001)화해마(P =0.001)균현저고우가수술조,compound C 조피질(P =0.005)화해마(P =0.017)균현저저우결혈재관주조。가수술조、결혈재관주조화 compound C 조피질 CytC 수평분별위0.496±0.278、1.461±0.321화1.018±0.175( F =19.915,P <0.001),해마분별위0.511±0.257、1.610±0.441화0.921±0.228(F =17.795,P <0.001),결혈재관주조피질(P <0.001)화해마(P <0.001) CytC 수평균현저고우가수술조,이 compound C 조피질(P =0.011)화해마(P =0.002)세포질 CytC수평균현저저우뇌결혈재관주조。결론억제 AMPK 활성능하조소서뇌결혈재관주후결혈측피질화해마세포질 CytC 표체。
Objective To investigate the effects of of inhibition of AMP-activated protein kinase (AMPK) on cytochrome c (CytC) expression in the cortex and hippocampus after focal cerebral ischemia-reperfusion in mice. Methods Thirty-six male C57BL/6 mice were randomly divided into 3 groups: a sham operation group, an ischemia-reperfusion group, and a compound C group (n = 12 in each group). The mice of the compound C group were intraperitonealy injected an AMPK specific inhibitor compound C (20 mg/kg) at the time of ischemia. A model of middle cerebral artery occlusion was induced by a modified suture method. After 24 h of reperfusion, Western blot was used to detect the expression levels of AMPK, phosphorylated-AMPK (p-AMPK), and cytoplasm CytC in the cortex and hippocampus in the ischemic side. Results p-AMPK/MPK levels in the cortex in the sham operation group, ischemia-reperfusion group, and compound C group were 0. 701 ± 0. 197, 1. 408 ± 0. 322, and 0. 930 ± 0. 229, respectively (F = 12. 000, P =0. 001); p-AMPK/MPK levels in the hippocampus were 0. 685 ± 0. 228, 1. 507 ± 0. 418, and 0. 964 ± 0. 378, respectively ( F = 8. 530, P = 0. 003 ); p-AMPK/AMPK levels both in the cortex ( P < 0. 001 ) and hippocampus (P = 0. 001) in the ischemia-reperfusion group were significantly higher than those in the sham operation group, p-AMPK/AMPK levels both in the cortex (P = 0. 005) and hippocampus (P = 0. 017) in the compound C group were significantly lower than those in the ischemia-reperfusion group. CytC levels in the cortex in the sham operation group, ischemia-reperfusion group, and compound C group were 0. 496 ±0. 278, 1. 461 ± 0. 321, and 1. 018 ± 0. 175, respectively (F = 19. 915, P < 0. 001); CytC levels in the hippocampus were 0. 511 ± 0. 257, 1. 610 ± 0. 441, and 0. 921 ± 0. 228 (F = 17. 795, P < 0. 001); CytC levels both in the cortex (P < 0. 001) and hippocampus (P < 0. 001) in the ischemia-reperfusion group were significantly higher than those in the sham operation group, while CytC levels both in the cortex (P = 0. 011) and hippocampus (P = 0. 002) in the compound C group were significantly lower than those in the ischemia-reperfusion group. Conclusion Inhibition of the AMPK may down-regulate the cytoplasm CytC expression in the cortex and hippocampus after cerebral ischemia-reperfusion in mice.