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

• Published in: Drug and chemical toxicology (New York, N.Y. 1978) Vol. 45; no. 5; pp. 2160 - 2168
• Main Authors: Erdogan, Mumin Alper, Yigitturk, Gurkan, Erbas, Oytun, Taskıran, Dilek
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 03.09.2022
• Subjects: Alzheimer's disease; dexpanthenol; hippocampus; memory impairment; neuroprotection; streptozotocin; Alzheimer’s disease; hippocampus; streptozotocin; memory impairment; neuroprotection; dexpanthenol
• ISSN: 0148-0545; 1525-6014; 1525-6014
• DOI: 10.1080/01480545.2021.1914464

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. 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-α) 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). It was observed that ICV-STZ significantly shortened PAL latency, increased levels of TNF-α in brain, decreased activity of ChAT in brain, and number of hippocampal neurons. However, dexpanthenol significantly reduced all of those STZ-induced harmful effects. 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.