Sugino T, Nozaki K, Tokime T, Hashimoto N, Kikuchi H
Department of Neurosurgery, Faculty of Medicine, Kyoto University, Japan.
Neurosci Lett. 1997 Nov 21;237(2-3):121-4. doi: 10.1016/s0304-3940(97)00827-6.
Impaired energy metabolism plays an important role in neuronal cell death after brain ischemia, and apoptosis has been implicated in cell death induced by metabolic impairment. In the present study, metabolic impairment was induced by 3-nitropropionic acid (3-NP), an irreversible inhibitor of succinate dehydrogenase. In order to clarify the involvement of poly(ADP-ribosyl)ation and apoptotic pathway in 3-NP induced cell death, we examined poly(ADP-ribosyl)ation and the apoptosis related gene protein expression after systemic administration of 3-NP by immunohistochemistry. Poly(ADP-ribosyl)ation was evidently detected in the striatal lesion but not in any other region. Immunoreactive ratio of Bcl-2 to Bax significantly increased both in the striatum and cortex. The data suggest that striatal cell death involves poly(ADP-ribosyl)ation and also apoptotic pathway in part following administration of 3-NP.
能量代谢受损在脑缺血后神经元细胞死亡中起重要作用，且细胞凋亡与代谢损伤诱导的细胞死亡有关。在本研究中，代谢损伤由琥珀酸脱氢酶的不可逆抑制剂3-硝基丙酸（3-NP）诱导。为了阐明聚（ADP-核糖）化和凋亡途径在3-NP诱导的细胞死亡中的作用，我们通过免疫组织化学检查了全身给予3-NP后聚（ADP-核糖）化和凋亡相关基因蛋白的表达。在纹状体病变中明显检测到聚（ADP-核糖）化，但在其他任何区域均未检测到。纹状体和皮质中Bcl-2与Bax的免疫反应比值均显著增加。数据表明，给予3-NP后，纹状体细胞死亡部分涉及聚（ADP-核糖）化以及凋亡途径。
