Ferrer I, López E, Blanco R, Rivera R, Ballabriga J, Pozas E, Martí E
Unitat de Neuropatologia, Servei d'Anatomia Patològica, Hospital Princeps d'Espanya, Hospitalet de Llobregat, Spain.
Exp Brain Res. 1998 Jul;121(2):167-73. doi: 10.1007/s002210050448.
Delayed neuronal death was produced in the CA1 area of the hippocampus following 5 min of forebrain ischemia in adult gerbils. Immunohistochemistry and Western blotting to Bcl-2, Bax, and Bcl-x was examined in control (age-matched, non-operated and sham-operated) and ischemic gerbils. Bcl-2 immunoreactivity was low in CA1 neurons, but Bax was highly expressed in CA1 neurons of control gerbils. Moderate Bcl-x immunoreactivity was observed in control CA1 neurons. Strong Bcl-2 and Bcl-x immunoreactivity was found in CA1 neurons following ischemia. Bcl-2, Bax, and Bcl-x were localized in dying cells, thus suggesting that expression of Bcl-2 was not sufficient to prevent nerve cells from dying. Although the Bcl-x antibody does not discriminate between Bcl-xL and Bcl-xS content in tissue sections, Western blots disclosed a marked increase in the intensity of the band corresponding to Bcl-xS, but not of the band corresponding to Bcl-xL in ischemic hippocampi, thus indicating that the increase in Bcl-xS is associated with delayed cell death following transient forebrain ischemia in the adult gerbil.
成年沙鼠前脑缺血5分钟后，海马CA1区出现延迟性神经元死亡。对对照（年龄匹配、未手术和假手术）和缺血沙鼠进行了针对Bcl-2、Bax和Bcl-x的免疫组织化学和蛋白质印迹检测。在对照沙鼠的CA1神经元中，Bcl-2免疫反应性较低，但Bax高度表达。在对照CA1神经元中观察到中等程度的Bcl-x免疫反应性。缺血后在CA1神经元中发现了强烈的Bcl-2和Bcl-x免疫反应性。Bcl-2、Bax和Bcl-x定位于死亡细胞，因此表明Bcl-2的表达不足以防止神经细胞死亡。尽管Bcl-x抗体不能区分组织切片中Bcl-xL和Bcl-xS的含量，但蛋白质印迹显示，在缺血海马中，对应于Bcl-xS的条带强度显著增加，而对应于Bcl-xL的条带强度未增加，因此表明Bcl-xS的增加与成年沙鼠短暂性前脑缺血后的延迟性细胞死亡有关。
