Safflower Yellow reduce lipid peroxidation, neuropathology, tau phosphorylation and improves amyloid β (1-42)-induced learning and memory impairment in rats
Safflower Yellow reduce lipid peroxidation, neuropathology, tau phosphorylation and improves amyloid β (1-42)-induced learning and memory impairment in rats
复制标题
红花黄减少脂质过氧化、神经病理学、tau 磷酸化并改善淀粉样蛋白 β (1-42) 诱导的大鼠学习和记忆障碍
DOI:
--
复制
发表时间:
2015
影响因子:
7.5
通讯作者:
Yan-li Hu
中科院分区:
文献类型:
--
作者:
Qin Ma;Ying-ying Ruan;Hui Xu;XuXiao-meng Shi;Yan-li Hu
Insoluble plaques of amyloid b proteins (Ab) and neurofibrillary tangles of hyperphosphorylated tau are key markers for Alzheimer’s disease (AD). Safflower yellow (SY) is one of traditional Chinese medicine extracted from safflower, which is suggested to have therapeutic potential for neurodegenerative.disorders. However, whether SY can ameliorate impairment of learning and memory in AD model, and its causal mechanism are still unclear. Here, we applied different doses of SY intragastrically to Wistar rats injected with amyloid b (1–42) for 1 month. By the Morris water maze test, we found that treatment of SY significantly attenuated amyloid b (1–42)-induced impairment of memory in rats. Mechanistically, SY treatment increased the level of superoxidedismutase (SOD) and Glutathione peroxidase (GSH-Px), and decreased the level of malondialdehyde (MDA) and acetylcholinesterase (T-CHE) in brain tissues of AD rats. Pathological analysis also showed that SY treatment inhibited the morphological alteration of neurons and tau hyperphosphorylation induced by amyloid b (1–42)-injection in the cortex and hippocampus. Moreover, SY treatment inhibited CDK-5 and GSK-3 signaling pathways, which are upregulated in AD rats. Our data indicate that safflower yellow can serve as a therapeutic candidate for Alzheimer’s disease.