The Effect of Lidocaine on the Experimental Model of Streptozotocin-Induced Alzheimer's Disease.
| Autor: | Tamam Y; Dicle University, Faculy of Medicine, Department of Neurology, Diyarbakır, Turkey., Yokuş B; Dicle University, Faculy of Veterinary Medicine, Department of Biochemistry, Diyarbakır, Turkey., Tamam C; Toros University, Faculty of Health Sciences, Mersin, Turkey., Yüceer H; İstanbul University, Aziz Sancar Institute of Experimental Medicine, Department of Neuroscience, İstanbul, Turkey., Karahan S; Dicle University, Faculy of Veterinary Medicine, Department of Laboratuvary Animals, Diyarbakır, Turkey., Em B; University of Health Sciences, Diyarbakır Gazi Yaşargil Training and Research Hospital, Diyarbakır, Turkey., Tamam ŞB; Neurologist Private Clinic, Adana, Turkey., Tüzün E; İstanbul University, Aziz Sancar Institute of Experimental Medicine, Department of Neuroscience, İstanbul, Turkey. |
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| Jazyk: | angličtina |
| Zdroj: | Noro psikiyatri arsivi [Noro Psikiyatr Ars] 2023 Feb 18; Vol. 60 (1), pp. 68-72. Date of Electronic Publication: 2023 Feb 18 (Print Publication: 2023). |
| DOI: | 10.29399/npa.28112 |
| Abstrakt: | Introduction: Alzheimer's disease (AD) is a neurodegenerative disease caused by the accumulation of amyloid plaques in the cerebral cortex and hippocampus. In this study, the effects of local anesthetic lidocaine on neurodegeneration markers and memory were investigated for the first time in streptozotocin-induced rat AD model. Methods: Streptozotocin (STZ) was administered intracerebroventricularly (ICV) into Wistar rats to develop AD model. For lidocaine group (n=14), lidocaine (5 mg/kg) was administered intraperitoneally (IP) in addition to STZ injection. Control group animals (n=9) were treated with saline for 21 days. Morris Water Maze (MWM) test was performed to evaluate memory after the injections were completed. Also, the serum levels of TAR DNA-binding protein-43 (TDP-43), amyloid precursor protein (APP), β-secretase 1, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), response element binding protein (CREB), c-FOS were measured using ELISA test and compared between groups. Results: Lidocaine group animals showed lower escape latency and time in quadrant scores in MWM inferring better memory performance. Furthermore, lidocaine administration caused a significant decline in TDP-43 levels. However, the expression of APP and β-secretase were significantly higher in AD and lidocaine groups compared to control group. Moreover, lidocaine group markedly had higher serum NGF, BDNF, CREB, and c-FOS levels compared to those in the AD group. Conclusion: In addition to neuroprotective effects in STZ-induced AD model, Lidocaine also appears to improve memory. This effect might be associated with increased levels of several growth factors and associated intracellular molecules. The therapeutic role of lidocaine in the pathophysiology of AD should be studied in the future. Competing Interests: Conflict of Interest: The authors declared that there is no conflict of interest. (Copyright: © 2023 Turkish Neuropsychiatric Society.) |
| Databáze: | MEDLINE |
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