中文摘要：

目的探究乳铁蛋白（LF）及张应力施加对成骨细胞成骨功能的影响。方法体外培养成骨细胞,随机分为7组：加LF组,加力组,加LF＋力组,加LF＋ERK1/2通路抑制剂组,加力＋ERK1/2通路抑制剂组,加LF＋力＋ERK1/2通路抑制剂组及空白对照组,采用茜素红染色检测细胞矿化能力的改变,PCR及Western Blot检测Col1、ALP、ERK1/2、P-ERK1/2分泌和蛋白表达的改变。结果 12h张应力加载下100ug/ml的LF能显著促进MC3T3-E1细胞矿化功能及Col1、ALP的m RNA和蛋白的表达,P-ERK1/2蛋白的表达也出现明显升高,而总蛋白ERK1/2未见明显变化。且加入ERK1/2通路抑制剂后,Col1、ALP、P-ERK1/2蛋白都出现显著降低。结论 LF的加入和张应力加载都可以促进MC3T3-E1细胞的成骨功能且可能有协同作用,二者的促进作用可能经过了ERK1/2信号通路的传导。

英文摘要：

Objective To investigate the influence of lactoferrin and tension stress on ossification of osteoblast. Methods Osteoblast were cultured in vitro and randomly divided into 7 groups： the group with lactoferrin, with tension stress, with lactoferrin and tension stress, with lactofetrin and inhibitors of ERK1/2 pathways, with tension stress and inhibitors of ERK1/2 pathways, with lactoferrin ,tension stress and inhibitors of ERK1/2 pathways, and control group. Observe the change of cell mineralization ability using alizarin red staining test, and the change of expression on Coil, ALP, ERK1/2 and P-ERKI/2 by using PCR and Western Blot. Results Under the tension stress for 12h, 1000ug/ml of lactoferrin could significantly promote the cell mineralization ability of MC3T3-E1 cells and the expression of Co11, ALP, mRNA and P-ERK 1/2, while ERK1/2 didn＇t change obviously. After adding inhibitors of ERK1/2 pathways, the expression of Coil, ALP and P-ERK1/2 were significantly reduced. Conclusion Lactoferrin and tension stress could promote the cell mineralization ability of MC3T3-E1 cells and they might achieve it synergistically. The promotion may be impacted through ERK1/2 pathways.