Nam Kwangwoo, Kimura Tsuyoshi, Kishida Akio
Division of Biofunctional Molecules, Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University, 2-3-10 Kanda-Surugadai, Tokyo 101-0062, Japan.
Biomaterials. 2007 Jan;28(1):1-8. doi: 10.1016/j.biomaterials.2006.08.002. Epub 2006 Sep 7.
2-methacryloyloxyethyl phosphorylcholine (MPC)-immobilized collagen gel was developed. Using 1-ethyl-3-(3-dimethyl aminopropyl)-1-carbodiimide hydrochloride (EDC) and N-hydroxysuccinimide (NHS), we cross-linked a collagen film in 2-morpholinoethane sulfonic acid (MES) buffer (EN gel). EN gel was prepared under both pH 4.5 and pH 9.0 in order to observe changes in cross-linking ability. To cross-link MPC to collagen gel, poly(MPC-co-methacrylic acid) (PMA) having a carboxyl group side chain was chosen. E/N gel was added to the MES buffer having pre-NHS activated PMA to make MPC-immobilized collagen gel (MiC gel). MiC gel was prepared under both acidic and alkaline conditions to observe the changes in the cross-linking ability of PMA. X-ray photoelectron spectroscopy showed that the PMA was cross-linked with collagen under both acidic and alkaline conditions. Differential scanning calorimetry (DSC) results showed that the shrinkage temperature increased for the MiC gels and that the increase would be greater for the MiC gel prepared under alkaline conditions. The data showed that swelling would be less when the MiC gel was prepared under alkaline conditions. The biodegradation caused by collagenase was suppressed for the MiC gel prepared under alkaline conditions due to stable inter- and intrahelical networks.
制备了固定有2-甲基丙烯酰氧乙基磷酰胆碱(MPC)的胶原凝胶。使用1-乙基-3-(3-二甲基氨基丙基)碳二亚胺盐酸盐(EDC)和N-羟基琥珀酰亚胺(NHS),我们在2-吗啉乙烷磺酸(MES)缓冲液中交联胶原膜(EN凝胶)。为了观察交联能力的变化,在pH 4.5和pH 9.0条件下制备EN凝胶。为了将MPC交联到胶原凝胶上,选择了具有羧基侧链的聚(MPC-共-甲基丙烯酸)(PMA)。将E/N凝胶加入到预先用NHS活化的PMA的MES缓冲液中,制成固定有MPC的胶原凝胶(MiC凝胶)。在酸性和碱性条件下制备MiC凝胶,以观察PMA交联能力的变化。X射线光电子能谱表明,PMA在酸性和碱性条件下均与胶原交联。差示扫描量热法(DSC)结果表明,MiC凝胶的收缩温度升高,且在碱性条件下制备的MiC凝胶的升高幅度更大。数据表明,在碱性条件下制备MiC凝胶时,其溶胀程度较小。由于稳定的螺旋间和螺旋内网络,碱性条件下制备的MiC凝胶对胶原酶引起的生物降解具有抑制作用。