Neuroprotective effects of dexpanthenol on streptozotocin-induced neuronal damage in rats

Autor: Mumin Alper Erdogan, Gurkan Yigitturk, Oytun Erbaş, Dilek Taskiran
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