Amentoflavone induces cell cycle arrest, apoptosis, and autophagy in BV-2 cells

被引:14
作者
Liu, Zheng [1 ,2 ]
Wang, Feng [1 ,2 ]
Ma, Hui [1 ]
Xia, Hechun [1 ]
Tian, Jihui [1 ]
Sun, Tao [1 ,2 ]
机构
[1] Ningxia Med Univ, Dept Neurosurg, Gen Hosp, 804 South Shengli St, Yinchuan 750004, Ningxia, Peoples R China
[2] Ningxia Med Univ, Incubat Base Natl Key Lab, Ningxia Key Lab Cerebrocranial Dis, Yinchuan 750004, Ningxia, Peoples R China
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2020年 / 25卷
基金
中国国家自然科学基金;
关键词
Epilepsy; Amentoflavone; BV-2; cells; Apoptosis; Cell cycle arrest; Autophagy; COLORECTAL-CANCER; EPILEPSY; PATHWAY; GROWTH; PROLIFERATION; INFLAMMATION; GENES; PHASE; NEUROPROTECTION; SUPPRESSION;
D O I
10.2741/4835
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Previous studies have shown that amentoflavone (AF) elicits anti-inflammatory and neuroprotective effects. To further investigate the effects of AF on the microglia cell line BV-2, proteomic analysis was performed to screen potential key regulators. The top 5 canonical pathways associated with AF treatment were EIF2 signaling, regulation of eIF4 and p70s6k signaling, mTOR signaling, protein ubiquitination pathway and phagosome maturation. The top up-regulated genes were DOCK2, SEC23A, ME1, UGGT1 and STOM, while the most down-regulated molecules were IGF2R, ATP5O, DDX47, WBP11 and IKBIP. AF significantly decreased BV-2 cell proliferation. It induced cell cycle arrest at G2/M, increased CDK2, p27Kip1 and p53/p-p53, and decreased CDK1/CDC2 and cyclin B1. Cell apoptosis was induced, with increased levels of BAX, c-caspase-3 and ccaspase-9, and decreased levels of BCL-XL. Increased level of autophagosome induced by AF was observed, and increased Beclin-1 and decreased phosphorylation of PI3K and Erk1 were found as well. In conclusion, AF induces cell cycle arrest at G2/M, promotes apoptosis and autophagy in BV-2 cells, which may account for the anti-inflammatory effect of AF in epilepsy.
引用
收藏
页码:798 / 816
页数:19
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