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中文摘要：
依"应力-生长关系"分析，应力刺激不足是损伤组织难以愈合和愈合迟缓的重要科学问题之一。根据力化学机制设想，利用细胞在力学过载下高表达的力生长因子MGF去刺激细胞，则损伤组织细胞在应力不足的条件下仍感受到力学过载信号而加速修复。本研究选择骨和韧带作为硬软两种组织的修复模型，重点研究其力生物学基础。考查力学刺激和MGF对成骨细胞、韧带成纤维细胞和骨髓间充质干细胞(MSC)细胞行为影响的异同，解析MGF作用机制；研制抗应力遮挡效应的MGF生物材料（MGF-聚乳酸、MGF-钛）及其骨固定和置换新装置，解析其抗应力遮挡效应；考查在防治失重性骨质疏松中MGF对骨质形成的影响并分析其细胞机制；研究MGF组合药物对韧带损伤修复的作用，采用MGF基因转染的MSC与支架复合，评价体内植入促进韧带损伤愈合的效果。本课题的成功研究将为骨和韧带缺损组织的功能性修复提供新举措，为微重力环境致骨质疏松防治提供新思路。
英文摘要：
Biomechanics；mechano-growth factor；bone tissue repair；ligament tissue repai；tissue engineering
结论摘要：
本项目选择骨和韧带作为硬软两种组织的修复模型，利用细胞生物学和分子生物学技术重点研究了其力生物学基础。(1) 研究了力学刺激和MGF 对成骨细胞、韧带成纤维细胞、肌腱细胞和骨髓间充质干细胞(MSCs)细胞行为的影响，解析MGF作用机制。发现拉伸刺激可提高成骨细胞MGF表达，MGF具有类似于机械拉伸的生物效应，可促成骨细胞早期增殖和增强成骨细胞分化，提示MGF可替代机械拉伸刺激。MGF可能通过诱导大鼠MSCs细胞骨架结构重构调控细胞生物力学特性，从而促进MSCs迁移。MGF通过FAK和ERK1/2信号途径改变大鼠肌腱细胞细胞骨架重排和细胞力学特性，促进细胞的迁移能力。MGF通过调控损伤后ACL细胞的细胞活力及胞外基质表达，可有效避免更严重的韧带撕裂损伤。(2) 研制了抗应力遮挡效应的MGF生物材料及其骨固定和置换新装置，解析其抗应力遮挡效应。结果表明MGF-聚乳酸促增殖和增强分化的活性的持续时间明显高于游离MGF。(3) 考察了在防治失重性骨质疏松中MGF对骨质形成的影响并分析其细胞机制，发现MGF能显著促进模拟微重力效应下成骨细胞增殖，并增加OCN表达量。MGF能提高大鼠松质骨的骨密度，部分对抗尾吊导致的松质骨骨密度丢失。包裹MGF的壳聚糖微球能促进MC3T3-E1类成骨细胞的增殖，延迟细胞的分化，表现出更持久的作用。(4) 在体实验证明了MGF在前交叉韧带和肌腱损伤修复中的作用。本项目的研究成果有望为骨和韧带缺损组织的功能性修复提供新举措，为微重力环境致骨质疏松防治提供新思路。
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期刊论文
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