Department of Physiology, Faculty of Medicine, Izmir Kâtip Çelebi University, Izmir, Turkey.
Department of Histology, Faculty of Medicine, Mugla University, Mugla, Turkey.
Drug Chem Toxicol. 2022 Sep;45(5):2160-2168. doi: 10.1080/01480545.2021.1914464. Epub 2021 Apr 20.
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 ( = 6), STZ + Saline ( = 6) and STZ + Dexpanthenol ( = 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.
虽然以记忆丧失为特征的最常见的与年龄相关的神经退行性疾病是阿尔茨海默病（AD），但目前只有对症治疗方法。最近提出了 AD 发病机制的一个复杂途径，其中包括炎症的增加。由于在以前的动物实验中，泛醇具有抗炎和神经保护作用，因此研究了泛醇在侧脑室（ICV）链脲佐菌素（STZ）诱导的散发性 AD（记忆障碍）动物模型中的作用和作用。
总共将 18 只成年 Sprague-Dawley 大鼠分为 3 组；对照组（n = 6）、STZ + 生理盐水（n = 6）和 STZ + 泛醇（n = 6）。通过立体定向术将 STZ（3 mg/kg）注入双侧脑室，将 12 只 AD 诱导大鼠分为两组，在 STZ 给药后 5 天：其中一组用泛醇（1000 mg/kg/天，腹腔注射）治疗 3 周，另一组用生理盐水治疗。治疗后进行被动回避学习（PAL）测试，然后提取所有动物的脑组织。测量脑肿瘤坏死因子-α（TNF-α）和胆碱乙酰转移酶（ChAT）水平，并使用 Cresyl 紫染色计数 Cornu ammonis-1（CA1）和 Cornu ammonis-3（CA3）中的神经元数量。
观察到 ICV-STZ 显著缩短 PAL 潜伏期，增加脑内 TNF-α水平，降低脑内 ChAT 活性，减少海马神经元数量。然而，泛醇显著降低了所有这些 STZ 诱导的有害作用。
泛醇通过减轻大鼠海马神经元丢失、胆碱能缺乏和神经炎症，显著防止了 ICV-STZ 引起的记忆障碍。这些发现表明，泛醇可能有益于治疗记忆障碍。
