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Lixisenatide Reduced Damage in Hippocampus CA1 Neurons in a Rat Model of Cerebral Ischemia-Reperfusion Possibly Via the ERK/P38 Signaling Pathway.
J Mol Neurosci. 2020 Jul; 70(7):1026-1037.JM

Abstract

Glucagon-like peptide-1 (GLP-1) is a gut-derived peptide that has various physiological actions. One of its main actions is the regulation of blood glucose level when it is elevated as it potentiates insulin release. It is also known that GLP-1 protects neurons from damage caused by neurodegenerative diseases. Lixisenatide is one of the GLP-1 analogues that has a strong affinity to the GLP-1 receptor. Experimental animal studies have shown that it holds a neuroprotective effect in Parkinson, myocardial, and cerebral ischemic disease animal models. The beneficial effect of lixisenatide on the brain after cerebral ischemia-reperfusion (I/R) is not clarified yet; thus, it needs further explanatory studies. Our research is the first to study the effect of lixisenatide on myeloperoxidase (MPO) and toll-like receptors (TLRs)/mitogen-activated protein kinase (MAPK) pathway in a rat model of cerebral I/R. Lixisenatide with 2 doses 0.7 and 7 nmol/kg was given intraperitoneal in 2 different groups for 14 days; then, the bilateral common carotid artery was occluded for 1 h followed by reperfusion for 1 h. Examination of hippocampus CA1 neurons by Nissl stain showed that the number of intact neurons was elevated in the lixisenatide-treated group related to the control group (I/R group). Lixisenatide exhibited neuroprotection action possibly via downregulation of MPO, TLR2/4, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and pP38 and upregulation of phosphorylated extracellular signal-regulated kinase (pERK1/2); thus, this study gives possible link between lixisenatide and TLR/MAPK pathway following cerebral I/R and supports the use of lixisenatide for neuroprotection against stroke.

Authors+Show Affiliations

Pharmacology and Toxicology Department, Faculty of Pharmacy, Helwan University, Cairo, 11795, Egypt. salma_nabil@pharm.helwan.edu.eg.Pharmacology and Toxicology Department, Faculty of Pharmacy, Helwan University, Cairo, 11795, Egypt.Pharmacology and Toxicology Department, Faculty of Pharmacy, Helwan University, Cairo, 11795, Egypt.Pharmacology and Toxicology Department, Faculty of Pharmacy, Helwan University, Cairo, 11795, Egypt.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32040827

Citation

Gad, Salma N., et al. "Lixisenatide Reduced Damage in Hippocampus CA1 Neurons in a Rat Model of Cerebral Ischemia-Reperfusion Possibly Via the ERK/P38 Signaling Pathway." Journal of Molecular Neuroscience : MN, vol. 70, no. 7, 2020, pp. 1026-1037.
Gad SN, Nofal S, Raafat EM, et al. Lixisenatide Reduced Damage in Hippocampus CA1 Neurons in a Rat Model of Cerebral Ischemia-Reperfusion Possibly Via the ERK/P38 Signaling Pathway. J Mol Neurosci. 2020;70(7):1026-1037.
Gad, S. N., Nofal, S., Raafat, E. M., & Ahmed, A. A. E. (2020). Lixisenatide Reduced Damage in Hippocampus CA1 Neurons in a Rat Model of Cerebral Ischemia-Reperfusion Possibly Via the ERK/P38 Signaling Pathway. Journal of Molecular Neuroscience : MN, 70(7), 1026-1037. https://doi.org/10.1007/s12031-020-01497-9
Gad SN, et al. Lixisenatide Reduced Damage in Hippocampus CA1 Neurons in a Rat Model of Cerebral Ischemia-Reperfusion Possibly Via the ERK/P38 Signaling Pathway. J Mol Neurosci. 2020;70(7):1026-1037. PubMed PMID: 32040827.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lixisenatide Reduced Damage in Hippocampus CA1 Neurons in a Rat Model of Cerebral Ischemia-Reperfusion Possibly Via the ERK/P38 Signaling Pathway. AU - Gad,Salma N, AU - Nofal,Shahira, AU - Raafat,Eman M, AU - Ahmed,Amany A E, Y1 - 2020/02/10/ PY - 2019/12/21/received PY - 2020/02/05/accepted PY - 2020/2/11/pubmed PY - 2020/2/11/medline PY - 2020/2/11/entrez KW - GLP-1 KW - Ischemia/reperfusion KW - Lixisenatide KW - TLR SP - 1026 EP - 1037 JF - Journal of molecular neuroscience : MN JO - J. Mol. Neurosci. VL - 70 IS - 7 N2 - Glucagon-like peptide-1 (GLP-1) is a gut-derived peptide that has various physiological actions. One of its main actions is the regulation of blood glucose level when it is elevated as it potentiates insulin release. It is also known that GLP-1 protects neurons from damage caused by neurodegenerative diseases. Lixisenatide is one of the GLP-1 analogues that has a strong affinity to the GLP-1 receptor. Experimental animal studies have shown that it holds a neuroprotective effect in Parkinson, myocardial, and cerebral ischemic disease animal models. The beneficial effect of lixisenatide on the brain after cerebral ischemia-reperfusion (I/R) is not clarified yet; thus, it needs further explanatory studies. Our research is the first to study the effect of lixisenatide on myeloperoxidase (MPO) and toll-like receptors (TLRs)/mitogen-activated protein kinase (MAPK) pathway in a rat model of cerebral I/R. Lixisenatide with 2 doses 0.7 and 7 nmol/kg was given intraperitoneal in 2 different groups for 14 days; then, the bilateral common carotid artery was occluded for 1 h followed by reperfusion for 1 h. Examination of hippocampus CA1 neurons by Nissl stain showed that the number of intact neurons was elevated in the lixisenatide-treated group related to the control group (I/R group). Lixisenatide exhibited neuroprotection action possibly via downregulation of MPO, TLR2/4, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and pP38 and upregulation of phosphorylated extracellular signal-regulated kinase (pERK1/2); thus, this study gives possible link between lixisenatide and TLR/MAPK pathway following cerebral I/R and supports the use of lixisenatide for neuroprotection against stroke. SN - 1559-1166 UR - https://www.unboundmedicine.com/medline/citation/32040827/Lixisenatide_Reduced_Damage_in_Hippocampus_CA1_Neurons_in_a_Rat_Model_of_Cerebral_Ischemia-Reperfusion_Possibly_Via_the_ERK/P38_Signaling_Pathway L2 - https://dx.doi.org/10.1007/s12031-020-01497-9 DB - PRIME DP - Unbound Medicine ER -
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