Kazak Filiz, Yarim Gul Fatma
Department of Biochemistry, Faculty of Veterinary Medicine, Mustafa Kemal University, Hatay, 31060, Turkey.
Department of Biochemistry, Faculty of Veterinary Medicine, Ondokuz Mayis University, Samsun, 55220, Turkey.
Neurosci Lett. 2017 Sep 29;658:32-36. doi: 10.1016/j.neulet.2017.07.059. Epub 2017 Aug 16.
Neuroinflammation is the inflammation of nervous tissue that can lead to neurodegeneration. Brain-derived neurotrophic factor (BDNF) is a neurotrophin which affects growth, function and survival of neurons, enhances the stabilization of synapses, regulates synaptic function and branching of dendrites and axons. Brain-derived neurotrophic factor is believed to be involved in the pathophysiology of central nervous system (CNS) diseases associated with neuroinflamation. The aim of this study was to investigate new protective and therapeutic effect of acetyl-l-carnitine (ALCAR) in neuroinflammation. Acetyl-l-carnitine was administered into Swiss Albino mice as 100mg/kg/day and 300mg/kg/day for 5days. Neuroinflammation was induced by lipopolysaccharide (LPS). Histopathological findings associated with ALCAR administration on neuroinflammation in the brain were determined. Moreover, the effects of ALCAR on BDNF concentration in the brain tissue was evaluated. The LPS administration showed higher microglial activation in the brain of LPS, 100A+LPS and 300A+LPS groups compared to that in the control (p<0.05). In the 100A+LPS group, microglial activation was lower and BDNF concentration was higher than in the 300A+LPS group (p>0.05). The findings suggest that the dose of ALCAR at 100mg/kg/day i.p. may have a beneficial effect on LPS-induced neuroinflammation in mice. As a conclusion, ALCAR may be used as an optional neuroprotective and therapeutic agent to attenuate inflammatory damage in the CNS regarding BDNF, in a dose dependent manner.
神经炎症是神经组织的炎症,可导致神经退行性变。脑源性神经营养因子(BDNF)是一种神经营养素,它影响神经元的生长、功能和存活,增强突触的稳定性,调节突触功能以及树突和轴突的分支。脑源性神经营养因子被认为参与了与神经炎症相关的中枢神经系统(CNS)疾病的病理生理过程。本研究的目的是探讨乙酰左旋肉碱(ALCAR)在神经炎症中的新的保护和治疗作用。将乙酰左旋肉碱以100mg/kg/天和300mg/kg/天的剂量给瑞士白化小鼠腹腔注射,持续5天。通过脂多糖(LPS)诱导神经炎症。确定了与ALCAR给药相关的脑组织神经炎症的组织病理学发现。此外,评估了ALCAR对脑组织中BDNF浓度的影响。与对照组相比,LPS组、100A+LPS组和300A+LPS组小鼠脑内小胶质细胞活化程度更高(p<0.05)。在100A+LPS组中,小胶质细胞活化程度低于300A+LPS组,BDNF浓度高于300A+LPS组(p>0.05)。这些发现表明,腹腔注射100mg/kg/天的ALCAR剂量可能对LPS诱导的小鼠神经炎症具有有益作用。总之,就BDNF而言,ALCAR可能作为一种可选的神经保护和治疗剂,以剂量依赖的方式减轻中枢神经系统的炎症损伤。