Department of Chemical Engineering and Materials Science, Michigan State University, East Lansing, MI 48824, USA.
J Biomater Sci Polym Ed. 2012;23(1-4):439-63. doi: 10.1163/092050610X552221. Epub 2011 Jan 28.
Experimentally induced axonal regeneration is compromised by glial scar formation arising from leptomeningeal fibroblasts cells in and around the hydrogel scaffold implanted for nerve repair. Strategies are needed to prevent such fibroblastic reactive cell layer formation for enhanced axonal regeneration. Here, we implement the technique of layer-by-layer assembled degradable, hydrogen bonded multilayers on agarose hydrogels to incorporate an anti-mitotic drug (1-β-D-arabinofuranosylcytosine (Ara-C)) within the agarose hydrogels. We show controlled release of Ara-C under physiological conditions over a period of days. The concentrations of Ara-C released from agarose at the different time points were sufficient to inhibit fibroblast growth in vitro, while not adversely affecting the viability of the neuronal cells.
实验诱导的轴突再生受到脑膜纤维母细胞在植入神经修复水凝胶支架内和周围形成的神经胶质瘢痕的影响。需要采取策略来防止这种成纤维细胞反应性细胞层的形成,以增强轴突再生。在这里,我们在琼脂糖水凝胶上实施层层组装可降解的氢键多层技术,将抗有丝分裂药物(1-β-D-阿拉伯呋喃糖基胞嘧啶(Ara-C))掺入琼脂糖水凝胶中。我们在几天的时间内展示了在生理条件下Ara-C 的控制释放。从琼脂糖在不同时间点释放的 Ara-C 浓度足以抑制体外成纤维细胞的生长,而不会对神经元细胞的活力产生不利影响。