Abstract
Lipid emulsion was recently shown to attenuate cell death caused by excitotoxic conditions in the heart. There are key similarities between neurons and cardiomyocytes, such as excitability and conductibility, which yield vulnerability to excitotoxic conditions. However, systematic investigations on the protective effects of lipid emulsion in the central nervous system are still lacking. This study aimed to determine the neuroprotective effects of lipid emulsion in an in vivo rat model of kainic acid-induced excitotoxicity through intrahippocampal microinjections. Kainic acid and/or lipid emulsion-injected rats were subjected to the passive avoidance test and elevated plus maze for behavioral assessment. Rats were sacrificed at 24 h and 72 h after kainic acid injections for molecular study, including immunoblotting and qPCR. Brains were also cryosectioned for morphological analysis through cresyl violet staining and Fluorojade-C staining. Anxiety and memory functions were significantly preserved in 1% lipid emulsion-treated rats. Lipid emulsion was dose-dependent on the protein expression of β-catenin and the phosphorylation of GSK3-β and Akt. Wnt1 mRNA expression was elevated in lipid emulsion-treated rats compared to the vehicle. Neurodegeneration was significantly reduced mainly in the CA1 region with increased cell survival. Our results suggest that lipid emulsion has neuroprotective effects against excitotoxic conditions in the brain and may provide new insight into its potential therapeutic utility.
Highlights
Excitotoxicity is considered a major mechanism underscoring neurodegenerative disorders involving functional loss and death of neurons in the central nervous system (CNS) [1,2]
Numerous therapeutic approaches have been investigated to terminate convulsive seizures induced by kainic acid (KA); the pursuit of appropriate remedies against neural damage induced by excitotoxic conditions is an ongoing endeavor
Molecular analysis, and morphological examinations, we propose that lipid emulsion (LE) provides neuroprotection against excitotoxicity in the brain
Summary
Excitotoxicity is considered a major mechanism underscoring neurodegenerative disorders involving functional loss and death of neurons in the central nervous system (CNS) [1,2]. Excitotoxic conditions have been implicated in acute and chronic neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and epilepsy [3]. KA-induced excitotoxicity in rodents results in deficient cognitive functions [7], elevated anxiety levels [8], and disruptive morphological changes in different areas of the brain [9,10]. Numerous therapeutic approaches have been investigated to terminate convulsive seizures induced by KA; the pursuit of appropriate remedies against neural damage induced by excitotoxic conditions is an ongoing endeavor
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