CAJ | 학술논문

目的观察全脑缺血/再灌注损伤后大鼠海马组织Bc12/腺病毒E1819kD相互作用蛋白3(BNIP3)表达水平的改变. 方法取10只成年雄性Wistar大鼠,采用随机数字表法分为假手术组和全脑缺血/再灌注72h组,每组5只.通过尼氏染色检测缺血模型是否引起海马神经元死亡.另取14只成年雄性Wistar大鼠采用随机数字表法分为假手术组(4只)、全脑缺血/再灌注1h组(5只)、全脑缺血/再灌注6h组(5只).在全脑缺血/再灌注后,于对应时间点取三组大鼠海马组织制备蛋白样品.western blot检测各时间点BNIP3表达水平的改变. 结果 (1)与假手术组比较,全脑缺血/再灌注72 h组中海马CAI区神经元形态不规则.细胞皱缩.胞核碎裂消失,表明海马神经元死亡.(2)大鼠海马组织BNIP3单体表达水平在全脑缺血/再灌注后上调,与假手术组相比.全脑缺血/再灌注1 h组(2.543±0.473)与全脑缺血/再灌注6 h组(2.942±0.777)的海马组织BNIP3单体蛋白表达水平都升高,差异有统计学意义(P<0.05).但全脑缺血/再灌注1 h组与全脑缺血/再灌注6 h组间比较差异无统计学意义(P>0.05).BNIP3双聚体在各时间点表达水平差异无统计学意义(P>0.05). 结论全脑缺血/再灌注损伤可以引起大鼠海马组织BNIP3单体表达水平上调.
목적 관찰전뇌결혈/재관주손상후대서해마조직Bc12/선병독E1819kD상호작용단백3(BNIP3)표체수평적개변. 방법 취10지성년웅성Wistar대서,채용수궤수자표법분위가수술조화전뇌결혈/재관주72h조,매조5지.통과니씨염색검측결혈모형시부인기해마신경원사망.령취14지성년웅성Wistar대서채용수궤수자표법분위가수술조(4지)、전뇌결혈/재관주1h조(5지)、전뇌결혈/재관주6h조(5지).재전뇌결혈/재관주후,우대응시간점취삼조대서해마조직제비단백양품.western blot검측각시간점BNIP3표체수평적개변. 결과 (1)여가수술조비교,전뇌결혈/재관주72 h조중해마CAI구신경원형태불규칙.세포추축.포핵쇄렬소실,표명해마신경원사망.(2)대서해마조직BNIP3단체표체수평재전뇌결혈/재관주후상조,여가수술조상비.전뇌결혈/재관주1 h조(2.543±0.473)여전뇌결혈/재관주6 h조(2.942±0.777)적해마조직BNIP3단체단백표체수평도승고,차이유통계학의의(P<0.05).단전뇌결혈/재관주1 h조여전뇌결혈/재관주6 h조간비교차이무통계학의의(P>0.05).BNIP3쌍취체재각시간점표체수평차이무통계학의의(P>0.05). 결론 전뇌결혈/재관주손상가이인기대서해마조직BNIP3단체표체수평상조.
Objective To study the changes in Bcl-2/adenovirus EIB 19kD-interacting protein 3(BNIP3)expression in the hippocampus of rats following transient forebmin ischemia. Methods Ten adult male Wistar rats were randomized into sham operation group(n=5)andischemia-rcperfosion group(n=5),and the rats in the latter group were subjectedto global ischemia for 15 min followed by repeffusion for 72 h.Nissl's staining was used to examine the neuronal death in the hippocampus induced by global brain isehemia.Another 14 adult male Wistar rats Were randomly divided into 3 groups,namely group 1 with sham operation(n=4),group 2 with global cerebral isehemia followed by reperfusion for 1 h(n=5),and group 3 with global isebemia and reperfusion for 6 h(n=5).All the rats were sacrificed to examine BNIP3 expression in the hippocampus using Western blotting. Results Compared with the sham operation group,the ischemia-reperfusion(72 h)group showed obvious neuronal death in the hippoeampal Cal region,where the neurons presented with irregular shape,cell shrinkage and nuclear fragmentation. BNIP3 monomer expression significantly increased in the hippocampus after isehemia-reperfusion in comparison with that in the sham operation group(P<0.05),but the length of reperfusion time(1 and 6 h)did not significantly affected BNIP3 monomer expression (2.543±0.473vs3 2.942±0.777,P>0.05).No significant difference was found in the expression level of BNIP3 dimers between the sham operation, ischemia-reperfusion 1 h and 6 h groups(P>0.05).Conclusion The expression of BNIP3 is up-regulated in the hippocampus of rats with transient forebrain ischemia.