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Mehrshad Mohammadzadeh@gmail.com 
, Zohreh Abdolmaleki , Ali Karimi Goudarzi , Seyed mohammadreza Bolandi
, Zohreh Abdolmaleki , Ali Karimi Goudarzi , Seyed mohammadreza Bolandi
Abstract: (25 Views)
Introduction/Background: Ischemic stroke and brain trauma are significant causes of death and disability in the West. Inflammasomes induce pro-inflammatory cytokine production in cerebral ischemia, thereby driving inflammation. The current study investigates the effects of glutamic acid, N-methyl-D-aspartate receptor agonist, and SH-SY5Y Neuroblastoma-Derived Exosomes in the rat model of cerebral ischemia.
Methods: Sixty adult male Wistar rats were randomly assigned to five groups. After MCAO, rats were treated with glutamic acid, SH-SY5Y neuroblastoma-derived exosomes, and both. The Garcia scale measured neurological damage 7 days after ischemia. We counted cell deaths in the brain using crystal violet staining. We examined gene and protein levels of BDNF, NLRP3, and NMDAR in brain tissue using real-time PCR and immunohistochemistry. The study used TTC staining to determine infarct cell volume in brain tissue, and ELISA tests to measure IL-1β and IL-18 levels.
Results: Cresyl violet staining demonstrated that glutamic acid+exosomes substantially reduced neurodegeneration. Garcia’s test results showed that glutamic acid, independently or in combination with exosomes, significantly enhanced the function of sensory and movement regions. The results clearly indicated that the expression of the BDNF gene and protein, as well as the NMDAR gene, increased, whereas the expression of the NLRP3 gene and protein, and the Caspase-1 protein, decreased. ELISA results showed a significant drop in IL-1β and IL-18 levels in MCAO groups treated with glutamic acid, exosomes, or both.
Conclusion: The use of glutamic acid with SH-SY5Y nueroblastoma-derived exosome exerts neuroprotective benefits by enhancing neurotorophic factors and diminishing apoptosis in the MCAO model.
Methods: Sixty adult male Wistar rats were randomly assigned to five groups. After MCAO, rats were treated with glutamic acid, SH-SY5Y neuroblastoma-derived exosomes, and both. The Garcia scale measured neurological damage 7 days after ischemia. We counted cell deaths in the brain using crystal violet staining. We examined gene and protein levels of BDNF, NLRP3, and NMDAR in brain tissue using real-time PCR and immunohistochemistry. The study used TTC staining to determine infarct cell volume in brain tissue, and ELISA tests to measure IL-1β and IL-18 levels.
Results: Cresyl violet staining demonstrated that glutamic acid+exosomes substantially reduced neurodegeneration. Garcia’s test results showed that glutamic acid, independently or in combination with exosomes, significantly enhanced the function of sensory and movement regions. The results clearly indicated that the expression of the BDNF gene and protein, as well as the NMDAR gene, increased, whereas the expression of the NLRP3 gene and protein, and the Caspase-1 protein, decreased. ELISA results showed a significant drop in IL-1β and IL-18 levels in MCAO groups treated with glutamic acid, exosomes, or both.
Conclusion: The use of glutamic acid with SH-SY5Y nueroblastoma-derived exosome exerts neuroprotective benefits by enhancing neurotorophic factors and diminishing apoptosis in the MCAO model.
Type of Manuscript: Experimental research article |
Subject:
Neurophysiology/Pharmacology
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