Amyloid β-peptides (Aβ) are considered as a major hallmark of Alzheimer's disease (AD) that can induce synaptic loss and apoptosis in brain regions, particularly in the cortex and the hippocampus. Evidence suggests that crocin, as the major component of saffron, can exhibit neuromodulatory effects in AD. However, specific data related to their efficacy to attenuate the synaptic loss and neuronal death in animal models of AD are limited. Hence, we investigated the efficacy of crocin in the CA3 and dentate gyrus (DG) regions of the hippocampus and also in frontal cortex neurons employing a rat model of AD. Male Wistar rats were randomly divided into control, sham, AD model, crocin, and AD model + crocin groups, with 8 rats per group. AD model was established by injecting Aβ1-42 into the frontal cortex rats, and thereafter the rats were administrated by crocin (30 mg/kg) for a duration of 12-day. The number of live cells, neuronal arborization and apoptosis were measured using a Cresyl violet, Golgi-Cox and TUNEL staining, respectively. Results showed that, the number of live cells in the hippocampus pyramidal neurons in the CA3 and granular cells in the DG regions of the AD rats significantly decreased, which was significantly rescued by crocin. Compared with the control group, the axonal, spine and dendrites arborization in the frontal cortex and CA3 region of the AD model group significantly decreased. The crocin could significantly reverse this arborization loss in the AD rats (P < 0.05). The apoptotic cell number in the CA3 and DG regions in the AD model group was significantly higher than that of the control group (P < 0.05), while crocin significantly decreased the apoptotic cell number in the AD group (P < 0.05). Conclusion. Crocin can improve the synaptic loss and neuronal death of the AD rats possibly by reducing the neuronal apoptosis.

中文翻译：

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藏红花素减轻阿尔茨海默病大鼠模型海马CA3区和额叶皮层齿状回和锥体神经元颗粒细胞损伤

淀粉样蛋白 β-肽 (Aβ) 被认为是阿尔茨海默病 (AD) 的主要标志，可诱导大脑区域的突触丧失和细胞凋亡，特别是在皮质和海马体中。有证据表明，藏红花的主要成分藏红花素可以在 AD 中表现出神经调节作用。然而，与它们在 AD 动物模型中减弱突触损失和神经元死亡的功效相关的具体数据是有限的。因此，我们使用 AD 大鼠模型研究了藏红花素在海马 CA3 和齿状回 (DG) 区域以及额叶皮层神经元中的功效。雄性Wistar大鼠随机分为对照组、假手术组、AD模型组、藏红花素组和AD模型+藏红花素组，每组8只。通过向额叶皮质大鼠注射Aβ1-42建立AD模型，然后给大鼠注射藏红花素（30mg/kg）12天。分别使用甲酚紫、高尔基-考克斯和 TUNEL 染色测量活细胞的数量、神经元分支和细胞凋亡。结果表明，AD大鼠CA3区海马锥体神经元活细胞数和DG区颗粒细胞数显着减少，这被藏红花素显着挽救。与对照组相比，AD模型组额叶皮层和CA3区的轴突、脊柱和树突分枝显着减少。藏红花素可以显着逆转 AD 大鼠的这种树枝化损失（P < 0.05）。AD模型组CA3区和DG区凋亡细胞数显着高于对照组（P < 0.05），而藏红花素显着降低AD组的凋亡细胞数（P < 0.05）。结论。藏红花素可能通过减少神经元凋亡来改善AD大鼠的突触丢失和神经元死亡。