Neuroscience Research Center and department of Physiology, Shiraz University of Medical sciences, Shiraz, Iran.
Eur J Pharmacol. 2010 May 25;634(1-3):84-8. doi: 10.1016/j.ejphar.2010.02.029. Epub 2010 Feb 23.
Neuroinflammation is associated with a number of neurodegenerative diseases. It is known that lipopolysaccharide (LPS) treatment induces neuroinflammation and memory deterioration. Agmatine, the metabolite of arginine by arginine decarboxylase, is suggested to be a neuroprotective agent. The aim of this study was to explore if agmatine can prevent LPS-induced spatial memory impairment and hippocampal apoptosis. Adult male Wistar rats (200-250 g) were trained in water maze for 4 days (3 days in hidden platform and the last day in visible platform task). Saline, LPS (250 microg/kg/ip) or (and) agmatine (5 or 10 mg/kg) were administered 4h before every training session. LPS treatment impaired water maze place learning while agmatine co-administration prevented it. Also western blot studies revealed that LPS induces hippocampal caspase-3 activation while agmatine treatment prevented it.
神经炎症与许多神经退行性疾病有关。已知脂多糖（LPS）处理会诱导神经炎症和记忆恶化。胍丁胺是精氨酸脱羧酶产生的精氨酸的代谢物，被认为是一种神经保护剂。本研究旨在探讨胍丁胺是否可以预防 LPS 诱导的空间记忆损伤和海马细胞凋亡。成年雄性 Wistar 大鼠（200-250g）在水迷宫中训练 4 天（3 天在隐藏平台，最后一天在可见平台任务）。盐水、LPS（250μg/kg/ip）或（和）胍丁胺（5 或 10mg/kg）在每次训练前 4 小时给药。LPS 处理损害了水迷宫空间学习，而胍丁胺共同给药则预防了这种损害。Western blot 研究还表明，LPS 诱导海马 caspase-3 激活，而胍丁胺处理则阻止了这种激活。
