中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (26): 4777-4780.doi: 10.3969/j.issn.1673-8225.2011.26.007

• 人工假体 artificial prosthesis • 上一篇    下一篇

红霉素、阿仑膦酸钠抑制磨损颗粒对小鼠巨噬细胞分泌白细胞介素1，6及肿瘤坏死因子α的影响

崔学生1，田  峰1，石玉泽1，张  帅1，金群华2   

  1. 1宁夏医科大学研究生院，宁夏回族自治区银川市   750004
    2宁夏医科大学附属医院骨3科，宁夏回族自治区银川市750004
  • 收稿日期:2011-01-09 修回日期:2011-03-21 出版日期:2011-06-25 发布日期:2011-06-25
  • 通讯作者: 金群华，教授，硕士生导师，宁夏医科大学附属医院骨3科，宁夏回族自治区银川市 750004 inqunhua@sina.com
  • 作者简介:崔学生★，男，1969年生，宁夏回族自治区银川市人，汉族，宁夏医科大学在读硕士，副主任医师，主要从事骨关节外科研究。现在银川市第二人民医院骨科工作。 hongxiexiashan@yahoo.cn
  • 基金资助:

    课题受“春晖计划”合作科研项目支持 ，编号：Z2008-1-75008，课题名称：红霉素和阿仑膦酸钠抑制磨损颗粒诱导小鼠骨溶解的实验研究。

Erythromycin and alendronate inhibition of wear particles influences macrophage secretion of interleukin 1, interleukin 2, and tumor necrosis factor alpha

Cui Xue-sheng1,Tian Feng1, Shi Yu-ze1, Zhang Shuai1, Jin Qun-hua2   

  1. 1Graduate School of Ningxia Medical University, Yinchuan  750001, Ningxia Hui Autonomous Region, China
    2Third Department of Orthopedics, Affiliated Hospital of Ningxia Medical University, Yinchuan  750004, Ningxia Hui Autonomous Region, China
  • Received:2011-01-09 Revised:2011-03-21 Online:2011-06-25 Published:2011-06-25
  • Contact: Jin Qun-hua, Professor, Master’s supervisor, Third Department of Orthopedics, Affiliated Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China jinqunhua@sina.com
  • About author:Cui Xue-sheng★, Studying for master’s degree, Associate chief physician, Now working at the Department of Orthopedics, the Second People’s Hospital of Yinchuan City, Graduate School of Ningxia Medical University, Yinchuan 750001, Ningxia Hui Autonomous Region, China hongxiexiashan@yahoo.cn
  • Supported by:

    the Chunhui Plan, No. Z2008-1-75008*

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摘要：

背景：阿仑膦酸钠的抗骨吸收作用是通过其对破骨细胞的抑制作用完成的，近年亦有报道证实红霉素有直接抑制破骨细胞的作用。
目的：观察阿仑膦酸钠和红霉素抑制钛颗粒刺激巨噬细胞分泌肿瘤坏死因子α、白细胞介素1，6的作用。
方法：分离、培养小鼠腹腔巨噬细胞，14 h后分为红霉素组及阿仑膦酸钠组，每组分为6个亚组。红霉素组：A组：仅为巨噬细胞；B组：巨噬细胞+钛颗粒；C组：巨噬细胞+钛颗粒+红霉素1 μg/L；D组：巨噬细胞+钛颗粒+红霉素10 μg/L；E组：巨噬细胞+钛颗粒+红霉素100 μg/L；F组：巨噬细胞+钛颗粒+红霉素1 000 μg/L。阿仑膦酸钠组分组及剂量同红霉素组。培养24 h后，用酶联免疫法检测细胞培养上清液中白细胞介素1，6及肿瘤坏死因子α的质量浓度。
结果与结论：B组白细胞介素1，6及肿瘤坏死因子α的质量浓度明显高于其他组(P < 0.05)，F组白细胞介素1，6及肿瘤坏死因子α的质量浓度明显低于C组(P < 0.05)。同剂量阿仑膦酸钠和红霉素组间差异无显著性意义(P > 0.05)。提示钛颗粒可以刺激巨噬细胞分泌大量的白细胞介素1，6及肿瘤坏死因子α，红霉素、阿仑膦酸钠能够呈剂量依赖型地有效抑制钛颗粒诱导的巨噬细胞分泌白细胞介素1，6及肿瘤坏死因子α。

关键词: 无菌性松动, 红霉素, 阿仑膦酸钠, 磨损颗粒, 巨噬细胞

Abstract:

BACKGROUND: Alendronate has an anti-bone resorption effect which is realized through its inhibitory effect on osteoclasts. Recently, it is confirmed that erythromycin plays a direct role against osteoclasts.
OBJECTIVE: To detect the effects of erythromycin and alendronate inhibited titanium (Ti) particles on interleukin 1(IL-1), IL-6 and tumor necrosis factor alpha (TNF-a) secreted from macrophages.
METHODS: Mouse peritoneal macrophages were separated and cultured, and then divided into erythromycin and alendronate groups. Each group was then divided into six subgroups. Erythromycin group: Group A was treated with macrophages alone, group B with macrophage+Ti particles, group C with macrophage+Ti particles+erythromycin (1μg/L), group D with macrophage+Ti particles+erythromycin (10 μg/L), group E with macrophage+Ti particles+erythromycin (100 μg/L), group F with macrophage+Ti particles+erythromycin (1 000 μg/L). The subgroups and dose of the alendronate group was the same as the erythromycin group. After 24 hours, the levels of IL-1, IL-6 and TNF-a in culture supernatant was detected by enzyme-linked immunosorbent assay.
RESULTS AND CONCLUSION: The levels of IL-1, IL-6 and TNF-a were much higher in groups B than those in other groups (P < 0 .05). The levels of IL-1, IL-6 and TNF-a were much lower in groups F than those in groups C (P < 0.05). The same dose of alendronate and erythromycin were not statistically significant (P > 0.05). It was shown that the Ti particles could stimulate macrophages to excrete a great amount of TNF-a ,IL-l and IL-6. Eythromycin and alendronate could significantly inhibit the production of IL-1, IL-6 and TNF-a secreted by Ti particles induced macrophages in a dose dependent manner.

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