Neuroprotective effects of acetyl-L-carnitine on lipopolysaccharide-induced neuroinflammation in mice: Involvement of brain-derived neurotrophic factor


KAZAK F., Yarım G. F.

NEUROSCIENCE LETTERS, cilt.658, ss.32-36, 2017 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 658
  • Basım Tarihi: 2017
  • Doi Numarası: 10.1016/j.neulet.2017.07.059
  • Dergi Adı: NEUROSCIENCE LETTERS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.32-36
  • Anahtar Kelimeler: Acetyl-L-carnitine, Brain derived neurotrophic factor, Lipopolysaccharide, Neuroinflammation, CENTRAL-NERVOUS-SYSTEM, ALZHEIMERS-DISEASE, GLIAL ACTIVATION, OXIDATIVE STRESS, MECHANISMS, REGENERATION, DYSFUNCTION, EXPRESSION, PLASTICITY, BARRIER
  • Ondokuz Mayıs Üniversitesi Adresli: Evet

Özet

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 100 mg/kg/day and 300 mg/kg/day for 5 days. 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 100 mg/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. (C) 2017 Elsevier B.V. All rights reserved.