Department of Psychiatry, Stritch School of Medicine, Loyola University Chicago, Loyola University Medical Center, 2160 South First Ave, Maywood, IL 60153, USA.
Neurotox Res. 2013 Aug;24(2):176-90. doi: 10.1007/s12640-013-9376-5. Epub 2013 Jan 19.
Agmatine is an endogenous brain metabolite, decarboxylated arginine, which has neuroprotective properties when injected intraperitoneally (i.p.) into rat pups following hypoxic-ischemia. A previous screen for compounds based on rat brain lysates containing agmatinase with assistance from computational chemistry, led to piperazine-1-carboxamidine as a putative agmatinase inhibitor. Herein, the neuroprotective properties of piperazine-1-carboxamidine are described both in vitro and in vivo. Organotypic entorhinal-hippocampal slices were firstly prepared from 7-day-old rat pups and exposed in vitro to atmospheric oxygen depletion for 3 h. Upon reoxygenation, the slices were treated with piperazine-1-carboxamidine or agmatine (50 μg/ml agents), or saline, and 15 h later propidium iodine was used to stain. Piperazine-1-carboxamidine or agmatine produced substantial in vitro protection compared to post-reoxygenated saline-treated controls. An in vivo model involved surgical right carotid ligation followed by exposure to hypoxic-ischemia (8 % oxygen) for 2.5 h. Piperazine-1-carboxamidine at 50 mg/kg i.p. was given 15 min post-reoxygenation and continued twice daily for 3 days. Cortical agmatine levels were elevated (+28.5 %) following piperazine-1-carboxamidine treatment with no change in arginine or its other major metabolites. Histologic staining with anti-Neun monoclonal antibody also revealed neuroprotection of CA1-3 layers of the hippocampus. Until endpoint at 22 days of age, no adverse events were observed in treated pups' body weights, rectal temperatures, or prompted ambulation. Piperazine-1-carboxamidine therefore appears to be a neuroprotective agent of a new category, agmatinase inhibitor.
胍丁胺是一种内源性脑代谢物,是精氨酸脱羧产物,在缺氧缺血后经腹腔(i.p.)注射到幼鼠体内具有神经保护作用。之前在计算化学的辅助下,基于大鼠脑匀浆中含有胍丁胺酶的化合物进行了筛选,导致哌嗪-1-羧酰胺被认为是一种潜在的胍丁胺酶抑制剂。本文描述了哌嗪-1-羧酰胺的体内外神经保护特性。首先从 7 日龄幼鼠中制备器官型海马齿状回切片,并在体外暴露于大气氧耗尽 3 小时。复氧后,用哌嗪-1-羧酰胺或胍丁胺(50μg/ml 试剂)或生理盐水处理切片,15 小时后用碘化丙啶染色。与复氧后用生理盐水处理的对照相比,哌嗪-1-羧酰胺或胍丁胺产生了显著的体外保护作用。体内模型涉及右侧颈总动脉结扎手术,然后暴露于缺氧缺血(8%氧气)2.5 小时。哌嗪-1-羧酰胺在复氧后 15 分钟以 50mg/kg i.p.给药,并连续 3 天每天两次给药。哌嗪-1-羧酰胺治疗后皮质胍丁胺水平升高(+28.5%),而精氨酸或其其他主要代谢物没有变化。用抗 Neun 单克隆抗体进行组织学染色也显示出海马 CA1-3 层的神经保护作用。在 22 天的观察期内,治疗组幼鼠的体重、直肠温度或自发活动均未出现不良事件。因此,哌嗪-1-羧酰胺似乎是一种新型神经保护剂,即胍丁胺酶抑制剂。