木犀草素
甲基乙二醛
细胞凋亡
PI3K/AKT/mTOR通路
活力测定
信号转导
化学
药理学
细胞生物学
类黄酮
生物
生物化学
抗氧化剂
酶
作者
Yi Liu,Jie Huang,Xian Zheng,Xia Yang,Yan Ding,Tongyong Fang,Yuyun Zhang,Shuaishuai Wang,Xiaofei Zhang,Xuan Luo,Anlei Guo,Kelly A. Newell,Yinghua Yu,Xu‐Feng Huang
标识
DOI:10.1038/s41598-017-08204-6
摘要
Methylglyoxal (MG) accumulation has been observed in human cerebrospinal fluid and body tissues under hyperglycaemic conditions. Recent research has demonstrated that MG-induces neuronal cell apoptosis, which promotes the development of diabetic encephalopathy. Our previous animal study has shown that luteolin, a natural flavonoid, attenuates diabetes-associated cognitive dysfunction. To further explore the neuroprotective properties of luteolin, we investigated the inhibitive effect of luteolin on MG-induced apoptosis in PC12 neuronal cells. We found that MG inhibited cell viability in a dose-dependent manner and induced apoptosis in PC12 cells. Pretreatment with Luteolin significantly elevated cell viability, reduced MG-induced apoptosis, inhibited the activation of the mTOR/4E-BP1 signaling pathway, and decreased pro-apoptotic proteins, Bax, Cytochrome C as well as caspase-3. Furthermore, we found that pretreatment with the mTOR inhibitor, rapamycin, significantly reduced the expression of the pro-apoptotic protein Bax. Therefore, these observations unambiguously suggest that the inhibitive effect of Luteolin against MG-induced apoptosis in PC12 cells is associated with inhibition of the mTOR/4E-BP1 signaling pathway.
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