Neuroprotective effects of dexpanthenol on streptozotocin-induced neuronal damage in rats
Autor: | Mumin Alper Erdogan, Gurkan Yigitturk, Oytun Erbaş, Dilek Taskiran |
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Rok vydání: | 2021 |
Předmět: |
dexpanthenol
Health Toxicology and Mutagenesis memory impairment Hippocampus Disease 010501 environmental sciences Pharmacology Toxicology streptozotocin 01 natural sciences Neuroprotection Pantothenic Acid Streptozocin Choline O-Acetyltransferase s disease Rats Sprague-Dawley Pathogenesis 03 medical and health sciences 0302 clinical medicine Alzheimer Disease Neuronal damage Animals Humans Medicine Memory impairment Rats Wistar Alzheimer’ Maze Learning 0105 earth and related environmental sciences Neurons Memory Disorders Chemical Health and Safety Tumor Necrosis Factor-alpha business.industry Public Health Environmental and Occupational Health Neurodegenerative Diseases General Medicine Streptozotocin Rats Disease Models Animal Neuroprotective Agents neuroprotection Dexpanthenol business 030217 neurology & neurosurgery medicine.drug |
Zdroj: | Drug and Chemical Toxicology. 45:2160-2168 |
ISSN: | 1525-6014 0148-0545 |
Popis: | Aim Although the most common age-related neurodegenerative disease defined by memory loss is Alzheimer's disease (AD), only symptomatic therapies are present. A complex pathway for the AD pathogenesis that includes an increase in inflammation has recently been suggested. Since in previous animal experiments dexpanthenol has anti-inflammatory and neuroprotective activities, effects and role of dexpanthenol in an intracerebroventricular (ICV)-streptozotocin (STZ) induced sporadic-AD(memory impairment) animal model have been examined. Design and methods In total, 18 adult sprague-dawley rats were classified into 3 groups; control (n = 6), STZ + Saline (n = 6) and STZ + Dexpanthenol (n = 6). Twelve AD-induced rats through STZ-injection (3 mg/kg) into both lateral ventricles via stereotaxy were separated into two groups five days after STZ administration: one of these groups was treated with dexpanthenol (1000 mg/kg/day, i.p.) for 3 weeks and the other with saline. A passive avoidance learning (PAL) test was used after treatment, followed by brain tissue extraction in all subjects. Brain levels of tumor necrosis factor-alpha (TNF-alpha) and choline acetyl transferase (ChAT) were measured and Cresyl violet staining was used to count neurons in cornu ammonis-1 (CA1) and cornu ammonis-3 (CA3). Results It was observed that ICV-STZ significantly shortened PAL latency, increased levels of TNF-alpha in brain, decreased activity of ChAT in brain, and number of hippocampal neurons. However, dexpanthenol significantly reduced all of those STZ-induced harmful effects. Conclusion Dexpanthenol significantly prevented the memory deficit induced by ICV-STZ through mitigating neuronal loss in hippocampus, cholinergic deficiency and neuroinflammation in rats. These findings suggest that dexpanthenol may be beneficial for treating memory impairment. |
Databáze: | OpenAIRE |
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