Nessren M Abd El-Rady1, Amel Ahmed2, Marwa Mahmoud Abdel-Rady3, Omnia I Ismail4. 1. Physiology Department, Faculty of Medicine, Assiut University, Assiut, Egypt. 2. Department of Histology and Cell Biology, Faculty of Medicine, Assiut University, Egypt. 3. Anesthesia and Intensive Care Department, Faculty of Medicine, Assiut University, Assiut, Egypt. 4. Department of Human Anatomy and Embryology, Faculty of Medicine, Assiut University, Assiut, Egypt.
Abstract
BACKGROUND: Alzheimer's disease (AD) is a worldwide severe medical and social burden. Liraglutide (LIR) has neuroprotective effects in preclinical animal models. AIM: To explore the probable neuroprotective impact of Glucagon-like peptide-1 (GLP-1) on rats' behavior and to elucidate its underlying mechanisms. METHODS: A total of 24 male albino rats were assigned to control, LIR (300 µg/kg subcutaneously (s.c.)), AD only (100 mg/kg aluminum chloride (AlCl3 ) orally) and LIR + AD treated groups. Eight radial arm maze was performed. Serum blood glucose, proinflammatory cytokines, oxidative stress markers were measured and hippocampal tissue homogenate neurotransmitters were evaluated. Histopathological and immunofluorescent examinations were performed. RESULTS: LIR prevents the impairment of learning and improves both working memory and reference memory through significant reduction of serum tumor necrosis factor (TNF-α), interleukin 6 (IL-6) and interferon-γ (INF-γ) and malondialdehyde (MDA) and through the increase of superoxide dismutase (SOD), dopamine, adrenaline, and noradrenaline. LIR also improves hippocampal histological features of ALCL3 administrated rats and decreases the percentage of neuronal loss. CONCLUSION: LIR normalizes ALCL3 -induced dementia. It improves cognitive dysfunction and ameliorates cerebral damage.
BACKGROUND:Alzheimer's disease (AD) is a worldwide severe medical and social burden. Liraglutide (LIR) has neuroprotective effects in preclinical animal models. AIM: To explore the probable neuroprotective impact of Glucagon-like peptide-1 (GLP-1) on rats' behavior and to elucidate its underlying mechanisms. METHODS: A total of 24 male albino rats were assigned to control, LIR (300 µg/kg subcutaneously (s.c.)), AD only (100 mg/kg aluminum chloride (AlCl3 ) orally) and LIR + AD treated groups. Eight radial arm maze was performed. Serum blood glucose, proinflammatory cytokines, oxidative stress markers were measured and hippocampal tissue homogenate neurotransmitters were evaluated. Histopathological and immunofluorescent examinations were performed. RESULTS: LIR prevents the impairment of learning and improves both working memory and reference memory through significant reduction of serum tumor necrosis factor (TNF-α), interleukin 6 (IL-6) and interferon-γ (INF-γ) and malondialdehyde (MDA) and through the increase of superoxide dismutase (SOD), dopamine, adrenaline, and noradrenaline. LIR also improves hippocampal histological features of ALCL3 administrated rats and decreases the percentage of neuronal loss. CONCLUSION: LIR normalizes ALCL3 -induced dementia. It improves cognitive dysfunction and ameliorates cerebral damage.
Authors: Samaila Musa Chiroma; Mohamad Taufik Hidayat Baharuldin; Che Norma Mat Taib; Zulkhairi Amom; Saravanan Jagadeesan; Mohd Ilham Adenan; Onesimus Mahdi; Mohamad Aris Mohd Moklas Journal: Int J Mol Sci Date: 2019-04-16 Impact factor: 5.923