SITAGLIPTIN MITIGATES SCOPOLAMINE-INDUCED NEUROCOGNITIVE DEFICITS VIA ACTIVATION OF Nrf2/HO-1 PATHWAY AND IMPROVED MITOCHONDRIAL ACTIVITY
Khodir, S., Gaafar, A., Mostafa, B., Abd El-aziz, N., Elfakhrany, A., Hassaan, S., Hassan, M., Abd EL-Khalek, S., El Menyawi, M. (2025). SITAGLIPTIN MITIGATES SCOPOLAMINE-INDUCED NEUROCOGNITIVE DEFICITS VIA ACTIVATION OF Nrf2/HO-1 PATHWAY AND IMPROVED MITOCHONDRIAL ACTIVITY. EKB Journal Management System, 25(1), 45-62. doi: 10.21608/ejfsat.2024.335654.1355
suzan A Khodir; Ahmad Gaafar; Basma Mostafa; Noha Abd El-aziz; amany Elfakhrany; Shehab Hassaan; Mai Hassan; Soha Abd EL-Khalek; Menna Allah El Menyawi. "SITAGLIPTIN MITIGATES SCOPOLAMINE-INDUCED NEUROCOGNITIVE DEFICITS VIA ACTIVATION OF Nrf2/HO-1 PATHWAY AND IMPROVED MITOCHONDRIAL ACTIVITY". EKB Journal Management System, 25, 1, 2025, 45-62. doi: 10.21608/ejfsat.2024.335654.1355
Khodir, S., Gaafar, A., Mostafa, B., Abd El-aziz, N., Elfakhrany, A., Hassaan, S., Hassan, M., Abd EL-Khalek, S., El Menyawi, M. (2025). 'SITAGLIPTIN MITIGATES SCOPOLAMINE-INDUCED NEUROCOGNITIVE DEFICITS VIA ACTIVATION OF Nrf2/HO-1 PATHWAY AND IMPROVED MITOCHONDRIAL ACTIVITY', EKB Journal Management System, 25(1), pp. 45-62. doi: 10.21608/ejfsat.2024.335654.1355
Khodir, S., Gaafar, A., Mostafa, B., Abd El-aziz, N., Elfakhrany, A., Hassaan, S., Hassan, M., Abd EL-Khalek, S., El Menyawi, M. SITAGLIPTIN MITIGATES SCOPOLAMINE-INDUCED NEUROCOGNITIVE DEFICITS VIA ACTIVATION OF Nrf2/HO-1 PATHWAY AND IMPROVED MITOCHONDRIAL ACTIVITY. EKB Journal Management System, 2025; 25(1): 45-62. doi: 10.21608/ejfsat.2024.335654.1355

SITAGLIPTIN MITIGATES SCOPOLAMINE-INDUCED NEUROCOGNITIVE DEFICITS VIA ACTIVATION OF Nrf2/HO-1 PATHWAY AND IMPROVED MITOCHONDRIAL ACTIVITY

The Egyptian Journal of Forensic Sciences and Applied Toxicology
Volume 25, Issue 1, March 2025, Page 45-62  XML PDF (1.55 MB)
Document Type: Original Article
DOI: 10.21608/ejfsat.2024.335654.1355
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Authors
suzan A Khodir email 1; Ahmad Gaafar2; Basma Mostafa3; Noha Abd El-aziz4; amany Elfakhrany5; Shehab Hassaan6; Mai Hassan7; Soha Abd EL-Khalek8; Menna Allah El Menyawi9
1physiology department, faculty of medicine, menoufia university
2Medical Physiology Department, Faculty of Medicine, Menoufia University
3Medical Biochemistry and Molecular Biology Department, Faculty of medicine, Menoufia University
4Anatomy and Embryology Department, Faculty of Medicine, Menoufia University
5Clinical Pharmacology Department, Faculty of medicine, Menoufia University
6Psychiatry department, Sulaiman Alrajhi University, Al Bukayriyah, Saudi Arabia. Psychiatry department, faculty of medicine, Assiut University, Assiut, Egypt.
7Anatomy and Embryology Department, Faculty of Medicine, Benha University
8Forensic Medicine and Clinical Toxicology department, Faculty of Medicine, Menoufia University
9Medical Physiology Department, Faculty of Medicine, Suez Canal University, Ismailia
Abstract
Background: Rats' memory is hampered by the muscarinic receptor antagonist scopolamine (Scop), which inhibits cholinergic neurotransmission. Objectives: to assess the protective impact of sitaglibtin and its underlying processes in neurocognitive impairments brought on by Scop. Methodology: Thirty adult male albino rats were divided into three groups: control, Scop, and Scop+STG (10/group). Rats were evaluated neurocognitively. The following were measured: BDNF, Nrf2, HO-1, citrate synthase (CS) activity, acetylcholine, MDA, SOD, TNF-α, interleukin (IL)-6, IL-10, and amyloid β 42 (Aβ42). Additionally, hippocampal histological and immunohistochemical analyses were performed. Results Along with significantly greater levels of MDA, TNF-α, IL-6, acetylcholine, and Aβ 42, as well as GFAP and Caspase-3 hippocampus immunoreaction, the Scop group also showed a decline in cognitive performance compared to control. Additionally, it down-regulated BDNF, Nrf2, and HO-1 gene expression in the hippocampus and markedly decreased IL-10, SOD, and CS activity. The Scop+STG showed a considerable amelioration in the neurocognitive deficits caused by Scop. Conclusion: In addition to up-regulating Nrf2 and HO-1 gene expressions, sitagliptin has a beneficial protective impact against Scop-induced cognition impairments through anti-oxidant, anti-inflammatory, enhanced mitochondrial activity, prevention of apoptosis, and neurotrophic actions.
Keywords
BDNF; Caspase-3; HO1; Nrf2; Scopolamine; Sitagliptin
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