中文摘要：

背景有钙化的墙的大多数胞虫包囊生物学上并且临床上沉默、不活跃。转变生长因素贝它(TGF-1 ) 1 在细胞的石灰化过程起一个关键作用。这研究的目的是估计在从肝的胞虫包囊孤立的胞虫 cysts.Methods Pericyst 房间的石灰化上发信号的 modulating TGF-1 的效果与 osteogenic 媒介是有教养的。这些房间为碱的磷酸酶活动和染色的矿化作用能力使用茜素红被估计。房间也与 recombinant 人 TGF-1 和 TGF- 禁止者，和表示被对待造骨细胞标记(RUNX2， osterix，和 osteocalcin ) 的侧面用西方的弄污被分析。禁止在 pericyst 墙的石灰化上发信号的 TGF-1 的效果在在 pericyst 以内的膀胱的 echinococcosis.Results 房间显示了的肝的一个现出症状之前的潜的疾病模型用 TGF- 禁止者的不同剂量被估计 7 个星期碱的磷酸酶活动和使矿物化的小瘤形成的高水平由 osteogenic 媒介导致了。造骨细胞标记(RUNX2， osterix，和 osteocalcin ) 的这些活动，以及表示侧面能被 recombinant 人 TGF-1 (rhTGF-1 ) 的增加禁止并且由 TGF- 禁止者提高了。在膀胱的包虫病的动物模型，表明 pericyst 墙的增加的石灰化的 TGF-1 的抑制，它与被联系减少了包囊负担索引和在 pericysts 以内的 protoscoleces.Conclusions 房间的更低的生存能力采用像造骨细胞的显型并且有 osteogenic 潜力。TGF-1 发信号的抑制增加胞虫包囊石灰化。在 pericysts 的石灰化的药理学调整可以是在胞虫疾病的治疗的一个新治疗学的目标。

英文摘要：

Background Most hydatid cysts with calcified walls are biologically and clinically silent and inactive. Transforming growth factor-beta 1 （TGF-β1） plays a critical role in the calcification process of cells. The aim of this study was to assess the effect of modulating TGF-β1 signaling on the calcification of hydatid cysts. Methods Pericyst cells isolated from hepatic hydatid cysts were cultured with osteogenic media. These cells were assessed for alkaline phosphatase activity and mineralization capacity using Alizarin Red staining. Cells were also treated with recombinant human TGF-β1 and TGF-β inhibitor, and the expression profiles of osteoblast markers （RUNX2, osterix, and osteocalcin） were analyzed using Western blotting. The effects of inhibiting TGF-β1 signaling on calcification of pericyst walls were assessed using different doses of TGF-β inhibitor for 7 weeks in a preclinical disease model of liver cystic echinococcosis. Results Cells within the pericyst displayed high levels of alkaline phosphatase activity and mineralized nodule formation, as induced by osteogenic media. These activities, as well as expression profiles of osteoblast markers （RUNX2, osterix, and osteocalcin） could be inhibited by addition of recombinant human TGF-β1 （rhTGF-β1） and enhanced by TGF-β inhibitor. In the animal model of cystic echinococcosis, inhibition of TGF-β1 signaling increased calcification of the pericyst wall, which was associated with decreased cyst load index and lower viability of protoscoleces. Conclusions Cells within the pericysts adopt an osteoblast-like phenotype and have osteogenic potential, inhibition of TGF-β1 signaling increases hydatid cyst calcification. Pharmacological modulation of calcification in pericysts may be a new therapeutic target in the treatment of hydatid disease.