PI3K/AKT/mTOR通路
下调和上调
免疫印迹
蛋白激酶B
细胞生物学
医学
分子生物学
化学
生物
信号转导
生物化学
基因
作者
Yan Sun,Junbo Ge,Weiwei Tang,Huanyu Hong,Dong Liu,Jiangtao Lin
出处
期刊:Biofactors
[Wiley]
日期:2021-01-25
卷期号:47 (3): 376-385
被引量:4
摘要
Abstract It is thought that maintaining preosteoblast viability is constructive to fracture healing. Here, we explored the effects of eupatilin on preosteoblast and addressed the mechanism associated with hsa_circ_0045714. Blood specimens were collected from 32 patients with hand fracture or calcaneus fracture. MC3T3‐E1 cells were treated with eupatilin. Small interfering‐RNA was transfected into MC3T3‐E1 cells. The ability of MC3T3‐E1 cells to survive, proliferate, migrate, and express fracture‐associated proteins was examined by 3‐(4,5)‐dimethylthiahiazo (‐z‐y1)‐3,5‐di‐ phenytetrazoliumromide (MTT), 5‐bromodeoxyuridine (BrdU), 24‐Transwell, Quantitative reverse transcription polymerase chain reaction (qRT‐PCR), and Western blot. Hsa_circ_0045714 was detected by qRT‐PCR. NF‐κB and PI3K/AKT were evaluated by Western blot. Eupatilin enhanced the survival, proliferation, and migration of MC3T3‐E1 cells. Cyclin D1, cyclin E, collagen II, aggrecan, and sulfated glycosaminoglycan (sGAG) were upregulated, while MMP‐13 was downregulated in eupatilin‐treated cells. Hsa_circ_0045714 was increased in patients with hand and calcaneus fractures with the time‐lapse of surgical operation. In eupatilin‐treated cells, Hsa_circ_0045714 was also elevated. However, the beneficial effects of eupatilin were weakened in hsa_circ_0045714‐deficient cells. Molecularly, eupatilin‐induced blockage of NF‐κB and activation of PI3K/AKT were abrogated in hsa_circ_0045714‐silenced cells. Our results confirmed the beneficial effects of eupatilin in preosteoblast, indicating eupatilin was a promising candidate for fracture healing.
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