Abstract

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-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).

Results

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.

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.

中文翻译：

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右泛醇对链脲佐菌素所致大鼠神经元损伤的保护作用

摘要

目标

虽然由记忆丧失定义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。最近提出了包括炎症增加在内的 AD 发病机制的复杂途径。由于在以前的动物实验中，右泛醇具有抗炎和神经保护活性，因此已经检查了右泛醇在脑室内 (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。

设计和方法

共18只成年sprague-dawley大鼠分为3组；对照 ( n  = 6)、STZ + 盐水 ( n  = 6) 和 STZ + 泛醇 ( n  = 6)。在 STZ 给药 5 天后，通过立体定向将 STZ 注射 (3 mg/kg) 到两个侧脑室的 12 只 AD 诱导大鼠分成两组：其中一组用右泛醇 (1000 mg/kg/天，ip) 治疗3周，另一个用生理盐水。治疗后使用被动回避学习（PAL）测试，然后在所有受试者中提取脑组织。测量脑内肿瘤坏死因子-α (TNF-α) 和胆碱乙酰转移酶 (ChAT) 的水平，并使用甲酚紫染色来计数cornu ammonis-1 (CA1) 和cornu ammonis-3 (CA3) 中的神经元。

结果

观察到 ICV-STZ 显着缩短 PAL 潜伏期，增加脑中 TNF-α 水平，降低脑中 ChAT 活性和海马神经元数量。然而，右泛醇显着降低了所有这些 STZ 诱导的有害影响。

结论

右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着预防 ICV-STZ 引起的记忆缺陷。这些发现表明，右泛醇可能有益于治疗记忆障碍。