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篇名
Vitisin B 經由雌激素受體調節Src 激酶及下游MAPK 之非基因型訊息路徑而刺激骨質新生
並列篇名
Vitisin B stimulates osteoblastogenesis via estrogen receptor-mediated activation of non-genomic Src and MAPKs pathway
作者 黃鈺玲黃齡丘邱文慧
中文摘要

Vitisin B 是小本山葡萄主要成分之一,民間常使用該本土植物於發炎性骨疾,宣稱可強壯筋骨。我們先前發現餵食富含vitisin B 的提取物可明顯改善卵巢切除鼠的骨質流失現象,現在進一步利用MC3T3-E1 造骨細胞,研究 vitisin B 對骨質新生的影響。結果發現與骨分化/ 成熟有關的鹼性磷解酶活性及礦化程度,均因處理vitisin B 而明顯提高。vitisin B 也使骨基質以及特有轉錄因子的表現量增加,且上述促進作用皆會被雌激素受體(ER)拮抗劑所抑制。不像典型的雌激素作用劑17-estradiol,vitisin B 不會刺激ER 或ER 調控的轉錄活性,但反而可快速磷酸化ER 受體及Src 激酶、繼而磷酸化p38 及ERK 這二個MAPK,這些作用也都會被ER 拮抗劑所抑制。進一步發現p38 及ERK 抑制劑會干擾vitisin B 誘導的造骨細胞分化,而 Src 抑制劑也會阻斷vitisin B 誘導的MAPK 活化與礦化。綜上,本研究發現vitisin B 具改善骨質流失的功效,其機轉可能是經由雌激素受體去活化細胞內非基因路徑的Src 激酶及下游的MAPK 訊息分子,進一步啟動造骨細胞特有的轉錄因子活化,繼而促進骨基質生成及礦化。

 

英文摘要

Background/Purpose: Vitisin B is a major component existed in Vitis thunbergii, a herbal medicine used in Taiwan for treatment of inflammatory bone diseases. We recently reported that vitisin B stimulated differentiation in primary cultured osteoblasts and treatment with vitisin B-enriched preparation obviously ameliorated ovariectomy-induced bone loss in mice. This study further delineated the action mechanism(s) that how vitisin B stimulates osteoblastogenesis by using MC3T3-E1 osteoblasts. Methods: Cell differentiation and mineralization were identified by alkaline phosphatase (ALP) activity and Alizarin red S staining, respectively. RT-PCR and western blot were used to analyze the expression of osteoblast-associated genes and signal molecules. The transcriptional activity of estrogen receptor (ER) was also assessed. Results: Vitisin B significantly increased ALP activity, bone mineralization, mRNA expression of osteoids (type 1 collagen, bone sialprotein and osteocalcin) and bone-characteristic transcription factors (runt-related transcription factor-2 and osterix) through ER since such responsiveness were obviously repressed by ER antagonist ICI182,780. Unlike 17β-estradiol (E2), vitisin B failed to stimulate either ERα- or ERβ-mediated transcriptional activity. Nevertheless, vitisin B rapidly induced ERα and Src phosphorylations within 5 min and evoked late phosphorylations of p38 and ERK after 15-30 min stimulation through ER. Furthermore, p38 inhibitor SB203580 and MEK inhibitor PD98059 significantly inhibited vitisin B induced differentiation. Src inhibitor PP2 significantly repressed vitisin B-induced activation of MAPK and finalmineralization suggesting that Src might play an important role. Conclusions: Vitisin B might act through ER-mediated activation of Src and downstream MAPK to stimulate osteoblastogenesis which contributed to its beneficial effect in prevent bone loss.

 

起訖頁 082-098
關鍵詞 雌激素受體造骨細胞Src 激酶vitisin Bestrogen receptorosteoblastSrc kinasevitisin B
刊名 中醫藥雜誌  
期數 201906 (30:1期)
出版單位 衛生福利部國家中醫藥研究所(原:國立中國醫藥研究所)
該期刊-上一篇 慢性腎絲球腎炎病人使用中藥之分析:基於醫院的橫斷面研究
該期刊-下一篇 臨床環境對針灸執業型態的影響:醫學中心與中醫醫院、診所之比較
 

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