Wang Han-Rui, Pei Si-Ying, Fan Dong-Xu, Liu Yan-Hui, Pan Xiao-Feng, Song Fan-Xu, Deng Shu-Hua, Qiu Hong-Bin, Zhang Ning
College of Basic Medicine, Jiamusi University, Jiamusi, Heilongjiang, China.
Department of Vascular Surgery, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang, China.
Evid Based Complement Alternat Med. 2020 Nov 30;2020:2861978. doi: 10.1155/2020/2861978. eCollection 2020.
The regulatory effect of luteolin on the progression of Alzheimer's disease (AD) remains unclear from the perspective of apoptosis. The present study aimed to investigate the protective effects of luteolin against A -induced cell apoptosis in pheochromocytoma (PC-12) cells. A was used to induce an in vitro model of AD. Estradiol was used as a positive control. The PC-12 cells were incubated with luteolin alone or in combination with fulvestrant or U0126. The results showed that luteolin treatment significantly prevents A -induced decrease in cell viability and inhibits A -induced cell apoptosis. After the addition of fulvestrant and U0126, the apoptosis rate of PC-12 cells increased significantly. In addition, luteolin treatment significantly upregulated the expression of Bcl-2 and downregulated the expression of Bax and caspase-3, whereas fulvestrant and U0126 partially reversed the effects of luteolin. Moreover, luteolin treatment upregulated the expression of ER and p-ERK1/2, whereas fulvestrant blocked the expression of p-ERK1/2. The study showed that luteolin could activate the ER/ERK/MAPK signalling pathway to protect PC-12 cells against A -induced cell apoptosis via selectively acting on ER. Thus, luteolin may be considered as a potential novel therapeutic strategy for AD.
从细胞凋亡的角度来看，木犀草素对阿尔茨海默病（AD）进展的调节作用尚不清楚。本研究旨在探讨木犀草素对Aβ诱导的嗜铬细胞瘤（PC-12）细胞凋亡的保护作用。Aβ被用于诱导AD的体外模型。雌二醇用作阳性对照。PC-12细胞单独用木犀草素处理，或与氟维司群或U0126联合处理。结果表明，木犀草素处理可显著防止Aβ诱导的细胞活力下降，并抑制Aβ诱导的细胞凋亡。加入氟维司群和U0126后，PC-12细胞的凋亡率显著增加。此外，木犀草素处理显著上调Bcl-2的表达，下调Bax和caspase-3的表达，而氟维司群和U0126部分逆转了木犀草素的作用。此外，木犀草素处理上调了ER和p-ERK1/2的表达，而氟维司群阻断了p-ERK1/2的表达。该研究表明，木犀草素可通过选择性作用于ER激活ER/ERK/MAPK信号通路，保护PC-12细胞免受Aβ诱导的细胞凋亡。因此，木犀草素可被视为一种潜在的AD新型治疗策略。
