Institute of Biomaterials and Surface Engineering, Key Laboratory for Advanced Technologies of Materials, Ministry of Education, Southwest Jiaotong University , Chengdu 610031, People's Republic of China.
ACS Appl Mater Interfaces. 2015 Feb 25;7(7):4423-32. doi: 10.1021/am509006y. Epub 2015 Feb 13.
Recently, UV irradiation has been reported as a new approach to significantly improve the anticoagulant properties of titanium dioxide (TiO2) films by suppressing fibrinogen adsorption and platelet adhesion. This study focuses on how fibrinogen adsorption of and platelet adhesion to TiO2 films is affected by the duration of UV irradiation. Furthermore, this study intends to describe the link between the suppression effect and the changes in the TiO2 films nature caused by photogenerated reactive oxygen species (ROS). First, we performed UV irradiation in different atmospheres as model 1 to determine the effect of oxygen gas on the anticoagulant properties of TiO2 films. The results showed that the suppression of platelet adhesion induced by UV irradiation depended on the presence of oxygen gas, indicating that ROS were photogenerated, and the ROS-induced surface change was related to the improvement in the anticoagulant ability. Then, we fabricated three other types of TiO2 samples in air by varying the UV irradiation time: (1) model 2, comprising fully UV-irradiated TiO2 films, (2) model 3, comprising partially UV-irradiated TiO2 films, and (3) model 4, comprising fully UV-irradiated TiO2-Si micropatterns. The results indicated that UV irradiation affected the anticoagulant properties of TiO2 films in a time-dependent manner. UV irradiation on TiO2 films for short duration (e.g., 1 min) evidenced a suppression effect on fibrinogen adsorption and platelet adhesion, an effect that could not be the result of photoinduced superhydrophilicity, increased hydroxyl groups (-OH) number, or decomposition of the adsorbed hydrocarbon. When the UV irradiation time was longer, this suppression effect extended from the surface of the UV-irradiated TiO2 films to the surface of the adjacent masked TiO2 films and the nearby Si surface. This result supported that the suppression effect could be related to the changes in the nature of the TiO2 films that were caused by the photogenerated and diffused ROS. Further, this extension of the suppression effect to the Si surface indicated that the photogenerated ROS could be used to improve the anticoagulant properties of other materials. A prolonged UV irradiation time (e.g., 240 min) may enhance the fibrinogen adsorption of and platelet adhesion to TiO2 films, which could be related to the decomposition of the adsorbed hydrocarbon and the increase in the positive charge. However, when comparing the enhancement effect and the suppression effect, the results showed that the latter was the main one to influence fibrinogen adsorption of and platelet adhesion to TiO2 films. This study provides an important basis for understanding the behavior of UV-irradiated TiO2 films as anticoagulant materials.
最近,有研究报道称,通过抑制纤维蛋白原吸附和血小板黏附,紫外线辐照可以显著提高二氧化钛(TiO2)薄膜的抗凝血性能。本研究主要关注紫外线辐照时间对 TiO2 薄膜的纤维蛋白原吸附和血小板黏附的影响,并旨在描述抑制效果与由光生活性氧(ROS)引起的 TiO2 薄膜性质变化之间的联系。首先,我们在不同气氛中进行紫外线辐照作为模型 1,以确定氧气对 TiO2 薄膜抗凝血性能的影响。结果表明,紫外线辐照诱导的血小板黏附抑制作用取决于氧气的存在,表明 ROS 被光生,ROS 诱导的表面变化与抗凝血能力的提高有关。然后,我们通过改变紫外线辐照时间在空气中制备了另外三种类型的 TiO2 样品:(1)模型 2,包含完全紫外线辐照的 TiO2 薄膜,(2)模型 3,包含部分紫外线辐照的 TiO2 薄膜,和(3)模型 4,包含完全紫外线辐照的 TiO2-Si 微图案。结果表明,紫外线辐照以时间依赖的方式影响 TiO2 薄膜的抗凝血性能。对 TiO2 薄膜进行短时间(例如 1 分钟)的紫外线辐照会对纤维蛋白原吸附和血小板黏附产生抑制作用,这种抑制效果不能归因于光诱导的超亲水性、增加的羟基(-OH)数量或吸附碳氢化合物的分解。当紫外线辐照时间更长时,这种抑制作用从紫外线辐照的 TiO2 薄膜表面扩展到相邻掩蔽的 TiO2 薄膜表面和附近的 Si 表面。这一结果支持抑制效果可能与由光生和扩散的 ROS 引起的 TiO2 薄膜性质变化有关。此外,这种抑制效果向 Si 表面的扩展表明,光生 ROS 可用于改善其他材料的抗凝血性能。延长紫外线辐照时间(例如 240 分钟)可能会增强 TiO2 薄膜的纤维蛋白原吸附和血小板黏附,这可能与吸附碳氢化合物的分解和正电荷的增加有关。然而,在比较增强效果和抑制效果时,结果表明后者是影响 TiO2 薄膜纤维蛋白原吸附和血小板黏附的主要因素。本研究为理解作为抗凝血材料的紫外线辐照 TiO2 薄膜的行为提供了重要依据。