l-Carnitine Inhibits Lipopolysaccharide-Induced Nitric Oxide Production of SIM-A9 Microglia Cells.
Emily L GillShreya RamanRichard A YostTimothy J GarrettVinata Vedam-MaiPublished in: ACS chemical neuroscience (2018)
Microglia are the resident immune effector cells of the central nervous system. They account for approximately 10-15% of all cells found in the brain and spinal cord, acting as macrophages, sensing and engaging in phagocytosis to eliminate toxic proteins. Microglia are dynamic and can change their morphology in response to cues from their milieu. Parkinson's disease is a neurodegenerative disease, associated with reactive gliosis, neuroinflammation, and oxidative stress. It is thought that Parkinson's disease is caused by the accumulation of abnormally folded alpha-synuclein protein, accompanied by persistent neuroinflammation, oxidative stress, and subsequent neuronal injury/death. There is evidence in the literature for mitochondrial dysfunction in Parkinson's disease as well as fatty acid beta-oxidation, involving l-carnitine. Here we investigate l-carnitine in the context of microglial activation, suggesting a potential new strategy of supplementation for PD patients. Preliminary results from our studies suggest that the treatment of activated microglia with the endogenous antioxidant l-carnitine can reverse the effects of detrimental neuroinflammation in vitro.
Keyphrases
- lipopolysaccharide induced
- inflammatory response
- induced apoptosis
- oxidative stress
- neuropathic pain
- lps induced
- spinal cord
- cell cycle arrest
- nitric oxide
- traumatic brain injury
- fatty acid
- signaling pathway
- dna damage
- systematic review
- newly diagnosed
- ischemia reperfusion injury
- patient safety
- ejection fraction
- hydrogen peroxide
- regulatory t cells
- cell death
- blood brain barrier
- quality improvement
- climate change
- amino acid
- heat shock
- small molecule
- pi k akt
- immune response
- nitric oxide synthase
- emergency medicine