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Sulforaphane Reverses the Amyloid-β Oligomers Induced Depressive-Like Behavior.
Journal of Alzheimer’s Disease ( IF 4 ) Pub Date : 2020-09-08 , DOI: 10.3233/jad-200397
Wei Wang 1, 2 , Cuibai Wei 1 , Meina Quan 1 , Tingting Li 1 , Jianping Jia 1, 2, 3, 4
Affiliation  

Background:Depression is one of the most common behavioral and psychological symptoms in people with Alzheimer’s disease (AD). To date, however, the molecular mechanisms underlying the clinical association between depression and AD remained elusive. Objective:Here, we study the relationship betweenmemory impairment and depressive-like behavior in AD animal model, and investigate the potential mechanisms. Methods:Male SD rats were administered amyloid-β oligomers (AβOs) by intracerebroventricular injection, and then the depressive-like behavior, neuroinflammation, oxidative stress, and the serotonergic system were measured in the brain. Sulforaphane (SF), a compound with dual capacities of anti-inflammation and anti-oxidative stress, was injected intraperitoneally to evaluate the therapeutic effect. Results:The results showed that AβOs induced both memory impairment and depressive-like behavior in rats, through the mechanisms of inducing neuroinflammation and oxidative stress, and impairing the serotonergic axis. SF could reduce both inflammatory factors and oxidative stress parameters to protect the serotonergic system and alleviate memory impairment and depressive-like behavior in rats. Conclusion:These results provided insights into the biological mechanisms underlying the clinical link between depressive disorder and AD, and offered new drug options for the treatment of depressive symptoms in dementia.

中文翻译:

萝卜硫素逆转淀粉样蛋白 β 寡聚体诱导的抑郁样行为。

背景:抑郁症是阿尔茨海默病 (AD) 患者最常见的行为和心理症状之一。然而,迄今为止,抑郁症和 AD 之间临床关联的潜在分子机制仍然难以捉摸。目的:在此,我们研究了 AD 动物模型中记忆障碍与抑郁样行为之间的关系,并探讨其潜在机制。方法:雄性SD大鼠通过脑室内注射β淀粉样蛋白寡聚体(AβOs),然后测量大脑中的抑郁样行为、神经炎症、氧化应激和5-羟色胺能系统。萝卜硫素(SF)是一种具有抗炎和抗氧化应激双重能力的化合物,腹腔注射以评估治疗效果。结果:结果表明,AβOs通过诱导神经炎症和氧化应激以及损害5-羟色胺能轴的机制,诱导大鼠记忆障碍和抑郁样行为。SF可以降低炎症因子和氧化应激参数,以保护5-羟色胺能系统,减轻大鼠的记忆障碍和抑郁样行为。结论:这些结果提供了对抑郁障碍与 AD 之间临床联系的生物学机制的见解,并为治疗痴呆的抑郁症状提供了新的药物选择。SF可以降低炎症因子和氧化应激参数,以保护5-羟色胺能系统,减轻大鼠的记忆障碍和抑郁样行为。结论:这些结果提供了对抑郁障碍与 AD 之间临床联系的生物学机制的见解,并为治疗痴呆的抑郁症状提供了新的药物选择。SF可以降低炎症因子和氧化应激参数,以保护5-羟色胺能系统,减轻大鼠的记忆障碍和抑郁样行为。结论:这些结果提供了对抑郁障碍与 AD 之间临床联系的生物学机制的见解,并为治疗痴呆的抑郁症状提供了新的药物选择。
更新日期:2020-09-08
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