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琥珀酸盐促进胶原蛋白矿化和牙本质修复。

Promotion of collagen mineralization and dentin repair by succinates.

机构信息

Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Clinical Research Center for Oral Diseases of Zhejiang Province, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Hangzhou, 310006, China.

Department of Chemistry, Zhejiang University, Hangzhou 310027, China.

出版信息

J Mater Chem B. 2022 Aug 4;10(30):5826-5834. doi: 10.1039/d2tb01005d.

DOI:10.1039/d2tb01005d
PMID:35876157
Abstract

Biomineralization of collagen fibers is regulated by non-collagenous proteins and small biomolecules, which are essential in bone and teeth formation. In particular, small biomolecules such as succinic acid (SA) exist at a high level in hard tissues, but their role is yet unclear. Here, our work demonstrated that SA could significantly promote intrafibrillar mineralization in two- and three-dimensional collagen models, where the relative mineralization rate was 16 times faster than the control group. Furthermore, the FTIR spectra and isothermal experimental results showed that collagen molecules could interact with SA a hydrogen bond and that the interaction energy was about 4.35 kJ mol. As expected, the SA-pretreated demineralized dentin obtained full remineralization within two days, whereas it took more than four days in the control group, and their mechanical properties were considerably enhanced compared with those of the demineralized one. The possible mechanism of the promotion effect of SA was ultimately illustrated, with SA modification strengthening the capacity of the collagen matrix to attract more calcium ions, which might create a higher local concentration that could accelerate the mineralization of collagen fibers. These findings not only advance the understanding of the vital role of small biomolecules in collagen biomineralization but also facilitate the development of an effective strategy to repair hard tissues.

摘要

胶原纤维的生物矿化受非胶原蛋白和小分子生物的调节,它们在骨骼和牙齿形成中至关重要。特别是,像琥珀酸(SA)这样的小分子在硬组织中含量很高,但它们的作用尚不清楚。在这里,我们的工作表明,SA 可以显著促进二维和三维胶原模型中的纤维内矿化,其中相对矿化率比对照组快 16 倍。此外,傅里叶变换红外光谱和等温实验结果表明,胶原蛋白分子可以与 SA 形成氢键,相互作用能约为 4.35 kJ/mol。正如预期的那样,经过 SA 预处理的脱矿质牙本质在两天内即可完全再矿化,而在对照组中则需要超过四天的时间,与脱矿质牙本质相比,其力学性能得到了显著提高。最终阐明了 SA 促进作用的可能机制,即 SA 修饰增强了胶原基质吸引更多钙离子的能力,这可能会产生更高的局部浓度,从而加速胶原纤维的矿化。这些发现不仅推进了对小分子在胶原生物矿化中重要作用的理解,也为开发有效的硬组织修复策略提供了帮助。

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