番红花苷
神经保护
超氧化物歧化酶
莫里斯水上航行任务
药理学
谷胱甘肽过氧化物酶
活性氧
化学
乙酰胆碱酯酶
抗氧化剂
生物化学
番红花
胆碱乙酰转移酶
生物
内分泌学
海马体
乙酰胆碱
植物
酶
作者
Chunyue Wang,X. Y. Cai,Wenjing Hu,Zhiping Li,Fange Kong,Xia Chen,Di Wang
标识
DOI:10.3892/ijmm.2018.4032
摘要
Due to its complex pathogenesis, the prevention and therapization of Alzheimer's disease (AD) remains a serious challenge. Crocin, the main compound isolated from Crocus sativus L., demonstrates various pharmacological activities including anti‑apoptotic properties. The present study investigated the neuroprotective effect of crocin and the underlying mechanisms. In l‑glutamate‑damaged HT22 cells, 3‑h crocin pretreatment strongly enhanced the HT22 cell viability, reduced the apoptotic rate, mitigated mitochondrial dysfunction, suppressed intracellular reactive oxygen species (ROS) accumulation and Ca2+ overload compared with untreated cells. Additionally, crocin significantly decreased the expression levels of Bax, Bad and cleaved caspase‑3 and increased the expression levels of B‑cell lymphoma‑extra large, phosphorylated (P‑) protein kinase B and P‑mammalian target of rapamycin compared with untreated cells. In mice with AD induced by d‑galactose and aluminum trichloride, crocin substantially improved the cognition and memory abilities of the mice as measured by their coordination of movement in an open field test, and reduced their escape time in the Morris water maze test compared with untreated mice. Biochemical analysis confirmed that crocin was able to reduce the Aβ1‑42 content in the mouse brains, increase the levels of glutathione peroxidase, superoxide dismutase, acetylcholine and choline acetyltransferase, and reduce the levels of ROS and acetylcholinesterase in the serum, cerebral cortex and hypothalamus compared with untreated mice. Immunohistochemical analysis demonstrated that crocin reduced Aβ1‑42 deposition in the hippocampus of the brains of treated mice compared with untreated mice. In conclusion, crocin demonstrates good prospects in the treatment of AD through the oxidative stress‑associated apoptosis signaling pathway.
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