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Neuroprotection from Excitotoxic Injury by Local Administration of Lipid Emulsion into the Brain of Rats

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Journal Int J Mol Sci
Publisher MDPI
Date 2020 Apr 17
PMID 32295117
Citations 3
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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.

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References
1.
Lee K, Park J, Won R, Lee H, Nam T, Lee B . Inhibition of hexokinase leads to neuroprotection against excitotoxicity in organotypic hippocampal slice culture. J Neurosci Res. 2010; 89(1):96-107. DOI: 10.1002/jnr.22525. View

2.
Inestrosa N, Varela-Nallar L . Wnt signaling in the nervous system and in Alzheimer's disease. J Mol Cell Biol. 2014; 6(1):64-74. DOI: 10.1093/jmcb/mjt051. View

3.
Cappuccio I, Calderone A, Busceti C, Biagioni F, Pontarelli F, Bruno V . Induction of Dickkopf-1, a negative modulator of the Wnt pathway, is required for the development of ischemic neuronal death. J Neurosci. 2005; 25(10):2647-57. PMC: 6725177. DOI: 10.1523/JNEUROSCI.5230-04.2005. View

4.
Shima A, Nitta N, Suzuki F, Laharie A, Nozaki K, Depaulis A . Activation of mTOR signaling pathway is secondary to neuronal excitability in a mouse model of mesio-temporal lobe epilepsy. Eur J Neurosci. 2015; 41(7):976-88. DOI: 10.1111/ejn.12835. View

5.
Li J, Iorga A, Sharma S, Youn J, Partow-Navid R, Umar S . Intralipid, a clinically safe compound, protects the heart against ischemia-reperfusion injury more efficiently than cyclosporine-A. Anesthesiology. 2012; 117(4):836-46. PMC: 3769111. DOI: 10.1097/ALN.0b013e3182655e73. View