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[1]陈德胜,张 晨,刘子歌,等.抑制 ERK 信号转导通路对磨损颗粒诱导炎性骨溶解的影响[J].宁夏医科大学学报,2021,(02):113-118.[doi:10.16050/j.cnki.issn1674-6309.2021.02.002]
　CHEN Desheng,ZHANG Chen,LIU Zige,et al.The Effect of Inhibition of ERK Signaling Pathway on Titanium Particles-induced Bone Grafting Air Pouch[J].Ningxia Medical University,2021,(02):113-118.[doi:10.16050/j.cnki.issn1674-6309.2021.02.002]
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抑制 ERK 信号转导通路对磨损颗粒诱导炎性骨溶解的影响(PDF)
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《宁夏医科大学学报》[ISSN:1005-8486/CN:64-1029/R]

卷:
期数:
2021年02期
页码:
113-118
栏目:
基础医学
出版日期:
2021-02-28

文章信息/Info

Title:
The Effect of Inhibition of ERK Signaling Pathway on Titanium Particles-induced Bone Grafting Air Pouch
文章编号:
1674-6309（2021）02-0113-06
作者:
陈德胜1;  张 晨2;  刘子歌2;  宋国瑞2;  郭凤英3;  李 燕3
（1. 宁夏医科大学总医院，银川 750004； 2. 宁夏医科大学临床医学院，银川 750004；3. 宁夏医科大学基础医学院，银川 750004）
Author(s):
CHEN Desheng1;  ZHANG Chen2;  LIU Zige2;  SONG Guorui2;  GUO Fengying3;  LI Yan3
（1. Department of Orthorpaedics， the General Hospital of Ningxia Medical University，Yinchuan 750004，China； 2. Clinical Medical College， Ningxia Medical University，Yinchuan 750004，China；3. Basic Medical College， Ningxia Medical University，Yinchuan 750004，China）
关键词:
骨溶解;  ERK信号转导通路;  PD98059; 植骨气囊动物模型
Keywords:
osteolysis; ERK signaling pathway; PD98059; bone grafting air pouch
分类号:
R683
DOI:
10.16050/j.cnki.issn1674-6309.2021.02.002
文献标志码:
A
摘要:
目的 探讨抑制细胞外调节蛋白激酶（ERK）信号转导通路对磨损颗粒诱导骨溶解的影响及可能的机制。方法 将45只小鼠随机分为空白对照组、钛颗粒刺激组和钛颗粒+ERK抑制剂组，每组15只。通过HE染色检测植入的小鼠颅骨及气囊壁组织中炎性反应情况；TRAP染色检测植入的小鼠颅骨及气囊壁组织中破骨细胞数目；免疫组化检测植入的小鼠颅骨及气囊壁组织中ERK及肿瘤坏死因子-α（TNF-α）蛋白阳性表达情况。结果 HE染色结果：与空白对照组比较钛颗粒刺激组组织标本中存在明显的炎性反应和大量炎性细胞浸润；与钛颗粒刺激组比较，钛颗粒+ERK抑制剂组炎性反应减弱，炎性细胞浸润减少。TRAP染色结果：钛颗粒刺激组阳性细胞数目多于空白对照组，钛颗粒+ERK抑制剂组阳性细胞数目相对于钛颗粒刺激组减少（P<0.05）。免疫组化染色结果：钛颗粒刺激组ERK及TNF-α阳性表达高于空白对照组，钛颗粒+ERK抑制剂组ERK及TNF-α阳性表达相对于钛颗粒刺激组减少（P<0.05）。结论 经ERK信号转导通路调控小鼠磨损颗粒诱导的骨溶解中ERK及其下游炎性因子TNF-α活性，从而可能影响破骨细胞的分化和活化，进而调控炎性骨溶解发生、发展。
Abstract:
Objective To investigate the effect of ERK signaling pathway inhibition on osteolysis induced by abrasive particles and its possible mechanism. Methods A total of 45 mice were randomly divided into control group（group A），titanium particle stimulation group（group B）and titanium particle + ERK inhibitor group（Group C），with 15 mice in each group.HE staining was used to detect the inflammatory reaction in the implanted mouse skull and the wall of airbag；Trap staining was used to detect the number of osteoclasts in the implanted mouse skull and the wall of airbag；Immunohistochemistry was used to detect the expression of ERK，TNF-α protein in the implanted mouse skull and the wall of airbag. Results HE staining results showed that compared with the blank control group，there were obvious inflammatory reaction and a large number of inflammatory cell infiltration in tissue samples of the titanium particle stimulation group.Compared with the titanium particle stimulation group，the inflammatory response and infiltration of inflammatory cells in the titanium particle + ERK inhibitor group decreased significantly.TRAP staining results showed that the number of positive cells in the titanium particle stimulation group was significantly higher than that in the blank control group（P＜0.05），while the number of positive cells in the titanium particle + ERK inhibitor group was significantly lower than that in the titanium particle stimulation group（P＜0.05）. Immunohistochemical staining results showed that the positive expression of ERK and TNF-αin the titanium granule stimulation group was significantly higher than that in the blank control group（P＜0.05），while the positive expression of ERK and TNF-α in the titanium particle + ERK inhibitor group was significantly lower than that in the titanium granule stimulation group（P＜0.05）. Conclusion The ERK signaling pathway regulates the activity of ERK and its downstream inflammatory factor TNF-α in osteolysis induced by wear particles in mice，which may affect the differentiation and activation of osteoclasts，and thus regulates the occurrence and development of inflammatory osteolysis.

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备注/Memo

备注/Memo:
收稿日期：2020-02-12
基金项目：国家自然科学基金（81760405；81760395；81560364）；宁夏自然科学基金重点项目（2018AAC02013）；宁夏医科大学校级课题重点项目（XZ2018014）
作者简介：陈德胜（1972—），男，教授，博士，硕士研究生导师，研究方向：人工关节临床与基础研究。
通信作者：李燕（1972—），女，教授，医学硕士，研究方向：人工关节基础研究。
更新日期/Last Update: 1900-01-01