Research articleNeuroprotective effects of acetyl-l-carnitine on lipopolysaccharide-induced neuroinflammation in mice: Involvement of brain-derived neurotrophic factor

- Acetyl-l-carnitine administration ameliorated LPS-induced neuroinflammation.
- Acetyl-l-carnitine increased the concentration of BDNF in the brain.
- Acetyl-l-carnitine may have protective and therapeutic potential for inflammation-related neurodegenerative diseases.

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.