Icaritin induces MC3T3-E1 subclone14 cell differentiation through estrogen receptor-mediated ERK1/2 and p38 signaling activation.
Icaritin induces MC3T3-E1 subclone14 cell differentiation through estrogen receptor-mediated ERK1/2 and p38 signaling activation.
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Icaritin 通过雌激素受体介导的 ERK1/2 和 p38 信号激活诱导 MC3T3-E1 亚克隆 14 细胞分化。
DOI：
10.1016/j.biopha.2017.07.071
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发表时间：
2017-10
期刊：
影响因子：
--
通讯作者：
Zhu Xiaofeng
中科院分区：
文献类型：
--
作者：
Wu Zhidi;Ou Ling;Wang Chaopeng;Yang Li;Wang Panpan;Liu Hengrui;Xiong Yingquan;Sun Kehuan;Zhang Ronghua;Zhu Xiaofeng
淫羊藿苷（Icaritin， ICT）是淫羊藿属淫羊藿苷的水解产物，具有多种药理和生物学活性。一些研究表明ICT具有潜在的骨保护作用，包括刺激成骨细胞分化和抑制破骨细胞分化。然而，ICT的这种合成代谢作用的分子机制在很大程度上仍然未知。在这里，我们发现ICT可以促进MC3T3-E1亚克隆14成骨前细胞的分化，并增加分化标志物碱性磷酸酶（ALP）、1型胶原（COL1）、骨钙素（OC）、骨钙蛋白（OPN）和矮子相关转录因子2 （RUNX2）的mRNA水平和蛋白表达，并改善矿化，骨结节形成和胶原合成证实了这一点。为了描述潜在的机制，我们研究了ICT对雌激素受体（ER）和丝裂原活化蛋白激酶（MAPK）信号传导的影响。ICT处理诱导p38激酶和细胞外信号调节激酶1/2 （ERK1/2）激活，但在同一时间点对c-Jun n -末端激酶（JNK）的激活没有影响。ER拮抗剂ICI182780、p38拮抗剂SB203580和ERK1/2拮抗剂PD98059显著抑制ict诱导的ALP、COL1、OC和OPN mRNA的表达。ICI182780可减弱ict诱导的p38和ERK1/2磷酸化。这些观察结果表明ICT成骨作用的潜在机制涉及ERK1/2和p38途径通过内质网激活。
Icaritin (ICT), a hydrolytic product of icariin from the genus Epimedium,has many indicated pharmacological and biological activities. Several studies have shown that ICT has potential osteoprotective effects, including stimulation of osteoblast differentiation and inhibition of osteoclast differentiation. However, the molecular mechanism for this anabolic action of ICT remains largely unknown. Here, we found that ICT could enhance MC3T3-E1 subclone 14 preosteoblastic cell differentiation associated with increased mRNA levels and protein expression of the differentiation markers alkaline phosphatase (ALP), type 1 collagen (COL1), osteocalcin (OC), osteoponin (OPN) and runt-related transcription factor 2 (RUNX2), and improved mineralization, confirmed by bone nodule formation and collagen synthesis. To characterize the underlying mechanisms, we examined the effect of ICT on estrogen receptor (ER) and mitogen-activated protein kinase (MAPK) signaling. ICT treatment induced p38 kinase and extracellular signal-regulated kinase 1/2 (ERK1/2) activation, but it demonstrated at the same time point no effect on activation of c-Jun N-terminal kinase (JNK). ER antagonist ICI182780, p38 antagonist SB203580 and ERK1/2 antagonist PD98059 markedly inhibited the ICT-induced the mRNA expression of ALP, COL1, OC and OPN. ICI182780 attenuated the ICT-induced phosphorylation of p38 and ERK1/2. These observations indicate a potential mechanism of osteogenic effects of ICT involving the ERK1/2 and p38 pathway activation through the ER.
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影响因子：
39.2
作者：
ALBRIGHT, F
通讯作者：
ALBRIGHT, F
影响因子：
5
作者：
Jiang, Ming-Chun;Chen, Xiao-Han;Chen, Wen-Fang
通讯作者：
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DOI：
10.1186/s13046-015-0133-x
发表时间：
2015-02-15
期刊：
Journal of experimental & clinical cancer research : CR
影响因子：
--
作者：
Wu T;Wang S;Wu J;Lin Z;Sui X;Xu X;Shimizu N;Chen B;Wang X
通讯作者：
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影响因子：
3.7
作者：
Hong J;Zhang Z;Lv W;Zhang M;Chen C;Yang S;Li S;Zhang L;Han D;Zhang W
通讯作者：
Zhang W
影响因子：
4.1
作者：
Kono, Shin-jiro;Oshima, Yasushi;Tanaka, Sakae
通讯作者：
Tanaka, Sakae