关键词: Alzheimer's disease Crocin inflammation pi3k/akt signaling

Mesh : Animals Alzheimer Disease / drug therapy metabolism Carotenoids / pharmacology administration & dosage Mice Cognitive Dysfunction / drug therapy etiology Proto-Oncogene Proteins c-akt / metabolism Phosphatidylinositol 3-Kinases / metabolism Hippocampus / drug effects metabolism Signal Transduction / drug effects Male Neuroprotective Agents / pharmacology administration & dosage Amyloid beta-Peptides / metabolism Neuroinflammatory Diseases / drug therapy Disease Models, Animal Peptide Fragments / pharmacology Maze Learning / drug effects Spatial Learning / drug effects Neurons / drug effects metabolism

来  源:   DOI:10.1002/brb3.3503   PDF(Pubmed)

Abstract:
BACKGROUND: Crocin has a good prospect in the treatment of Alzheimer\'s disease (AD), but the mechanisms underlying its neuroprotective effects remain elusive. This study aimed to investigate the neuroprotective effects of Crocin and its underlying mechanisms in AD.
METHODS: AD mice were set up by injecting Aβ25-35 solution into the hippocampus. Then, the AD mice were injected intraperitoneally with 40 mg/kg/day of Crocin for 14 days. Following the completion of Crocin treatment, an open-field test, Y-maze test and Morris water maze test were conducted to evaluate the impact of Crocin on spatial learning and memory deficiency in mice. The effects of Crocin on hippocampal neuron injury, proinflammatory cytokine expressions (IL-1β, IL-6, and TNF-α), and PI3K/AKT signaling-related protein expressions were measured using hematoxylin and eosin staining, Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR) experiments, respectively.
RESULTS: Crocin attenuated Aβ25-35-induced spatial learning and memory deficiency and hippocampal neuron injury. Furthermore, the Western blot and qRT-PCR results showed that Crocin effectively suppressed inflammation and activated the PI3K/AKT pathway in Aβ25-35-induced mice.
CONCLUSIONS: Crocin restrained neuroinflammation via the activation of the PI3K/AKT pathway, thereby ameliorating the cognitive dysfunction of AD mice.
摘要:
背景:藏红花素在阿尔茨海默病(AD)的治疗中具有良好的前景,但是其神经保护作用的潜在机制仍然难以捉摸。本研究旨在探讨藏红花素对AD的神经保护作用及其机制。
方法:AD小鼠通过向海马注射Aβ25-35溶液来建立。然后,AD小鼠腹腔注射40mg/kg/天的藏红花素14天。在完成藏红花治疗后,露天测试,采用Y迷宫试验和Morris水迷宫试验评价藏红花素对小鼠空间学习记忆障碍的影响。藏红花素对海马神经元损伤的影响,促炎细胞因子表达(IL-1β,IL-6和TNF-α),使用苏木精和伊红染色检测PI3K/AKT信号相关蛋白的表达,蛋白质印迹,和定量实时聚合酶链反应(qRT-PCR)实验,分别。
结果:藏红花素减轻了Aβ25-35诱导的空间学习记忆缺陷和海马神经元损伤。此外,Westernblot和qRT-PCR结果显示,藏红花素有效抑制Aβ25-35诱导小鼠的炎症反应,激活PI3K/AKT通路。
结论:藏红花素通过激活PI3K/AKT通路抑制神经炎症,从而改善AD小鼠的认知功能障碍。
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