Elucidation of tendon calcification inhibition mechanism of histamine H2-receptor antagonist

组胺H2受体拮抗剂抑制肌腱钙化机制的阐明

• 批准号: 23592159
• 负责人: YAMAMOTO Kenichi
• 金额: $ 3.16万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23592159/
• 关键词: 異所性石灰化; 異所性骨化; H2ブロッカー; 石灰化抑制; ｔｔｗ; 腱石灰化; Famotidine; Histamine; ttw; 国際情報交流 アメリカ; 国際研究者交流 アメリカ

Although there are many clinical reports that histamine H2-receptor antagonists (H2 blockers) is effective for the treatment of calcific tendinitis and ossification differentiation previously, there is no report about the basic research, the mechanism. We investigated the basic mechanisms of calcification inhibition of the tendon through the H2 blockers in this study. We selected the famotidine for H2 blocker and administrated to the osteoblast cell line MC3T3-E1 and tendon-derived cell lines TTD6 and conformed that famotidine suppressed the calcification in vitro. Next we demonstrated that by using a mouse TTW ,ectopic calcification occurs in the Achilles' tendon in vivo and famotidine suppressed the ectopic calcification. The effect of famotidine for ectopic calcification was also demonstrated on basic medicine.

虽然此前有很多临床报道称组胺H2受体拮抗剂（H2阻滞剂）治疗钙化性肌腱炎和骨化分化有效，但其基础研究、作用机制尚无报道。在这项研究中，我们通过H2阻滞剂研究了肌腱钙化抑制的基本机制。我们选择法莫替丁作为H2阻滞剂，分别给药于成骨细胞系MC3T3-E1和肌腱源性细胞系TTD6，证实法莫替丁对体外钙化有抑制作用。接下来，我们通过小鼠TTW证明，体内跟腱发生异位钙化，法莫替丁抑制异位钙化。法莫替丁治疗异位钙化的效果也在基础医学上得到证实。