摘要
目的观察含铜不锈钢对血管内皮细胞黏附、增殖及凋亡的影响,并与316L不锈钢进行比较。方法将血管内皮细胞接种于两种材料表面,在培养1、2、3 d后,应用吖啶橙染色及甲基噻唑基四唑(MTT)法检测细胞在两种材料表面黏附和增殖活性。并制备两种材料的浸提液,用浸提液培养血管内皮细胞,采用流式细胞术检测细胞凋亡率。结果荧光显微镜下,细胞在两种材料表面均伸展良好,呈铺路石状生长。在培养1、2 d时,含铜不锈钢组黏附的细胞数多于316L不锈钢组(P<0.05);3 d时两组间差异无统计学意义(P>0.05)。MTT结果显示,含铜不锈钢组在1、2 d的吸光度值高于316L不锈钢组,差异有统计学意义(P<0.05);而在培养3 d后,两组间差异无统计学意义(P>0.05)。316L不锈钢组的早期凋亡率高于含铜不锈钢组,差异有统计学意义(P<0.05)。结论含铜不锈钢较316L不锈钢更利于血管内皮细胞的黏附及增殖,并可以降低血管内皮细胞的早期凋亡率。
Objective To observe the influence of copper-bearing stainless steel on adhesion, proliferation and apoptosis of vascular endothelial cell (VEC). Methods The samples of two kinds of materials were inoculated with VEC and incubated for 1, 2 and 3 d. After stained by acridine orange, the cells adhered on the surface of samples were observed under a fluorescent microscope. The proliferation of VEC was detected by methyl thiazolyl tetrazolium (MTT) test. Next, leaching liquor of these two kinds of materials was prepared and used to culture VEC. The apop- tosis of VEC was measured by flow cytometry. Results Fluorescent microscope showed VEC spread into fusiform shape, copper-bearing stainless steel surfaces had a significantly higher number of adherent VEC than 316L stainless steel at 1 and 2 d (/0〈0.05). No significant difference of adherent VEC was observed between two kinds of materials at 3 d (P〉0.05). MTY results indicated that the optical density (OD) value of copper-bearing stainless steel were higher than that of 316L stainless steel at 1 and 2d(P〈0.05). No significant difference of OD value was observed between two kinds of materials at 3 d(P〉0.05). The early apoptosis ratio of 316L stainless steel was higher than copper-bearing stainless steel (P〈0.05). Conclusion Copper-bearing stainless steel could promote the adhesion, proliferation of VEC, and inhibit the early apoptosis ratio of VEC.
出处
《华西口腔医学杂志》
CAS
CSCD
北大核心
2013年第1期17-20,25,共5页
West China Journal of Stomatology
基金
国家自然科学基金资助项目(51171186)
辽宁省科技计划基金资助项目(2010225025)
关键词
含铜不锈钢
血管内皮细胞
黏附
增殖
细胞凋亡
copper-bearing stainless steel
vascular endothelial cell
adhesion
proliferation
apoptosis