首页 / 院系成果 / 成果详情页

Beta-Ecdysone Protects Mouse Osteoblasts from Glucocorticoid-Induced Apoptosis In Vitro 期刊论文

编号：

b67a3fe5-3335-48d4-b001-3194a55b4286
作者：

Dai, WeiWei#*^[1,2]Wang, LiBo(王利波)#^[1]Jin, GuoQin(金国琴)^[3]Wu, HongJin^[1];Zhang, Jie^[1];Wang, ChengLong^[1];Wei, YuanJi^[1];Lee, JoonHo^[1];Lay, YuAn Evan^[2];Yao, Wei^[2];
语种：

英文
期刊：

PLANTA MEDICA ISSN：0032-0943 2017 年 83 卷 11 期 (888 - 894) ; JUL
收录：
关键词：

glucocorticoid osteoporosis beta-ecdysone apoptosis gene expression
摘要：

Glucocorticoid-induced osteoporosis is a common form of secondary osteoporosis. Glucocorticoids affect both bone formation and resorption, and prolonged glucocorticoid exposure can suppress osteoblast activities. beta-Ecdysone, found in many plants, is involved in protein synthesis, carbohydrate and lipid metabolism, and immunologicmodulation. Here, we evaluated the effects of beta-ecdysone on osteoblast viability by assessing apoptosis following treatment with excess glucocorticoids. Mouse bone marrow stromal cells were induced to differentiate and grow into osteoblasts, and then treated with 10 mu M glucocorticoid and 10, 1, or 0.1 mu M beta-ecdysone. The expression levels of osteoblast growth and differentiation factors (runt-related transcription factor 2, osteogenic protein-1, and alkaline phosphatase), apoptosis-related genes (transformation- related protein 53, ataxia telangiectasia mutated protein, caspase-3, and caspase-8), and Akt1 and phospho-Akt (Thr308) were then assessed via alkaline phosphatase staining, acridine orange-propidium iodide staining, annexin V/ PI apoptosis assay, real-time RT-PCR, and Western blot analyses. Notably, treatment with 10 mu M glucocorticoid resulted in reduced osteoblast viability and the specific activity of alkaline phosphatase as well as reduced runt-related transcription factor 2, osteogenic protein-1, and alkaline phosphatase mRNA expression in vitro, indicating that glucocorticoid inhibited osteogenic differentiation. Moreover, glucocorticoid treatment yielded increased transformation-related protein 53, ataxia telangiectasia mutated protein, caspase-3, and caspase-8 expression and decreased Akt1 and phospho-Akt levels, indicating glucocorticoid-induced apoptosis. Meanwhile, beta-ecdysone inhibited glucocorticoid function, preserving the expression of Akt1 and phospho-Akt and reducing the expression of transformation-related protein 53, ataxia telangiectasia mutated protein, caspase-3, and caspase-8. Thus, beta-ecdysone prevented glucocorticoid-induced osteoblast apoptosis in vitro. These data highlight the potential for beta-ecdysone as a
推荐引用方式
GB/T 7714：

Dai Wei-Wei,Wang Li-Bo,Jin Guo-Qin, et al. Beta-Ecdysone Protects Mouse Osteoblasts from Glucocorticoid-Induced Apoptosis In Vitro [J].PLANTA MEDICA,2017,83(11):888-894.
APA：

Dai Wei-Wei,Wang Li-Bo,Jin Guo-Qin,Wu Hong-Jin,&Yao Wei.(2017).Beta-Ecdysone Protects Mouse Osteoblasts from Glucocorticoid-Induced Apoptosis In Vitro .PLANTA MEDICA,83(11):888-894.
MLA：

Dai Wei-Wei, et al. "Beta-Ecdysone Protects Mouse Osteoblasts from Glucocorticoid-Induced Apoptosis In Vitro" .PLANTA MEDICA 83,11(2017):888-894.
条目包含文件：

文件类型：PDF,文件大小：

正在加载全文

未找到全文

浏览次数：64  下载次数：0

分享到：

浏览次数：64

下载次数：0

打印次数：0