Document Type : Review Article
Authors
1
Medical Physiology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt.
2
Histology and Cell Biology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia
3
Medical Biochemistry and Molecular Biology Department, Faculty of medicine, Menoufia University
4
Histology and Cell Biology, Faculty of Medicine, Assiut University, Assiut, 71515, Egypt.
5
Medical Physiology Department, Faculty of Medicine, Suez Canal University
6
Neuropsychiatry Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia
7
Human Anatomy and Embryology, Faculty of Medicine, Assiut University, Assiut, 71515, Egypt.
8
Medical Pharmacology Department, Faculty of medicine, Suez Canal University Ismailia, Egypt
Abstract
Abstract
Introduction: Cognitive deficits and aging were evoked by D-galactose (D-gal). Fasudil (Fsd) slows the start and progress of neurodegenerative illnesses.
Objective: to illustrate the neuroprotective effect of Fsd in D-gal induced cognitive deficits and the underling mechanisms involved
Material & methods: Thirty Wister albino male rats divided into control, D-gal, D-gal+Fsd groups. Rats were subjected to MWM, NOR and EPM tests then rats were sacrificed and MDA, catalase, TNF-α, IL-6 hippocampal gene expression of BDNF, SIRT1 and NF-kB were assessed. Histopathological and immunoreaction for caspase-3 and GFAP were done.
Results: D-gal revealed cognitive impairment, with substantial elevation of MDA, TNF-α, IL-6 and NF-kB gene expression and significant reduction of catalase, SIRT1 and BDNF gene expression of D-gal with upregulation of caspase-3 and GFAP immunoreaction in hippocampus. Fsd dramatically improved D-gal induced changes.
Conclusion: Fsd alleviated D-gal induced cognitive deficits by anti-oxidant, anti-inflammatory, anti-apoptotic mechanisms in addition to up-regulation of Sirt1 and BDNF gene expression and improving gliosis.
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