Notoginsenoside R1 functionalized gelatin hydrogels to promote reparative dentinogenesis
Notoginsenoside R1 functionalized gelatin hydrogels to promote reparative dentinogenesis
复制标题
三七皂苷R1功能化明胶水凝胶促进修复性牙本质生成
DOI：
10.1016/j.actbio.2020.12.031
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发表时间：
2021-02-16
影响因子：
9.7
通讯作者：
Pan, Yihuai
中科院分区：
文献类型：
--
作者：
Wang, Lei;Fu, Hui;Pan, Yihuai
纸浆封面材料通常在诊所中采用，以形成修复性牙本质，从而保护牙髓组织免受龋齿，意外暴露的果肉或部分肺门切开术的病例。诊所中使用的一些传统的纸浆封盖材料包括氢氧化钙和三氧化钙聚集体。但是，稀薄的修复性牙本质存在局限性，需要很长时间才能导致牙髓变性变化。在本文中，开发了可注射的胶体凝胶，以通过甲基丙烯酸官能化明胶的简单紫外线方法诱导修复性牙本质的形成，该方法载有Notoginsenosenoside R1（Gel-MA/NGR1）。物理化学性质检查的结果表明，制备的凝胶-MA/NGR1水凝胶具有适当的相互连接的多孔微体系结构，孔径为10.5微米，合适的机械性能，模量为50-60 kPa，可实现细胞粘附和增殖。水凝胶保持亲水性，并具有持续的药物释放性能。此外，凝胶-MA/NGR1通过升高牙齿核标记物ALP和OCN的表达水平以及细胞外基质矿化，从而显着增强了小鼠牙乳头细胞的牙遗传学分化。通过将前体注射到Sprague-Dawley大鼠的预售肺泡腔中，进行体内刺激，然后立即进行原位紫外线交联。结果表明，凝胶-MA/NGR1具有促进修复性牙本质形成的强大能力。甲莫妥蛋白和曙红，Masson和免疫组织化学染色（DMP-1，DSPP，OCN和RUNX2）和Micro-CT被用来说明牙齿发生的有效性，并且发现钙化的相对体积的相对量增加了类似于175倍。所有结果表明，凝胶-MA/NGR1水凝胶促进了修复性牙本质的形成，这表明该水凝胶具有巨大的潜力，作为造成牙本质形成的纸浆限制材料。意外暴露的果肉。但是，较薄的修复性牙本质存在局限性，需要很长时间才能在传统的纸浆封盖材料中导致牙髓牙髓变化。在本文中，我们报告了一种出乎意料的急性纸浆盖材料，用于通过甲基丙烯酸（MA）功能化的明胶（Gel-MA/NGR1）功能化明胶的简单紫外线方法来诱导修复性牙本质的形成。结果表明，凝胶-MA/NGR1具有促进修复性牙本质形成的强大能力（钙化的相对体积与175倍相似）。我们的工作为临床应用提供了另一个潜在的选择。 （c）2020 Acta Mitalietia Inc.由Elsevier Ltd.保留所有权利。
Pulp-capping materials are commonly adopted in the clinic to form reparative dentin and thus protect dental pulp tissues from cases of deep caries, accidentally exposed pulps or partial pulpotomy. Some traditional pulp capping materials used in the clinic include calcium hydroxide and mineral trioxide aggregates. However, there are limitations to thin restorative dentin, and a long period of time is needed to cause degenerative changes in dental pulp. In this paper, injectable colloidal gels were developed to induce the formation of reparative dentin through a simple UV method from methacrylic acid functionalized gelatin loaded with notoginsenoside R1 (Gel-MA/NGR1). The results of the physicochemical property examinations showed that the prepared Gel-MA/NGR1 hydrogel possessed an appropriate interconnected porous microarchitecture with a pore size of 10.5 micrometres and suitable mechanical properties with a modulus of 50-60 kPa, enabling cell adhesion and proliferation. The hydrogel remained hydrophilic with sustained drug release performance. In addition, Gel-MA/NGR1 significantly enhanced the odontogenetic differentiation of mouse dental papilla cells by elevating the expression levels of the dentinogenic markers ALP and OCN and extracellular matrix mineralization. In vivo stimulation was carried out by injecting the precursors into the predrilled alveolar cavity of Sprague-Dawley rats followed by immediate in situ UV crosslinking. The results showed that Gel-MA/NGR1 has a strong capacity to promote reparative dentin formation. Haematoxylin& eosin, Masson, and immunohistochemical staining (DMP-1, DSPP, OCN and RUNX2) and micro-CT were employed to illustrate the effectiveness of dentinogenesis, and the relative volumes of calcification were found to have increased similar to 175-fold. All of the results showed that the Gel-MA/NGR1 hydrogel promoted reparative dentin formation, which suggests that this hydrogel provides great potential as a pulp-capping material to induce dentin formation.Statement of significancePulp capping therapy is required to treat deep dental caries and accidentally exposed pulp. However, there are limitations to thin restorative dentin and a long period of time is needed to cause degenerative changes in dental pulp for traditional pulp capping materials. In this paper, we report an unexpected, acute pulp capping material for inducing the formation of reparative dentin through a simple UV method from methacrylic acid (MA) functionalized gelatin loaded with NGR1 (Gel-MA/NGR1). The results showed that the Gel-MA/NGR1 has a strong capacity to promote reparative dentin formation (the relative volumes of calcification increased similar to 175 fold). Our work provides another potential choice for clinical application. (C) 2020 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.