CX3CR1对创伤性骨髓炎大鼠骨骼肌微纤维、ERK/MAPK信号通路及炎症反应的影响  

Effects of CX3CR1 on skeletal muscle microfibers,ERK/MAPK signaling pathway and inflammatory response in rats with traumatic osteomyelitis

作　　者：曹众 李春燕 鲁广生 周琦石 CAO Zhong;LI Chunyan;LU Guangsheng;ZHOU Qishi(Department of Orthopedics,Dongguan Taixin Hospital,Dongguan 523000,China.)

机构地区：[1]东莞台心医院骨科,广东省东莞市523000

出　　处：《组织工程与重建外科》2024年第1期58-63,共6页Journal of Tissue Engineering and Reconstructive Surgery

基　　金：国家自然科学基金(81674001)。

摘　　要：目的探索CX3CR1对创伤性骨髓炎大鼠骨骼肌微纤维、ERK/MAPK信号通路及炎症反应的影响。方法选取30只SPF级SD雄性大鼠,依据随机数字表法分为健康组、模型组、CX3CR1抑制组,每组10只。除健康组外,其余各组均建立创伤性骨髓炎模型。其中健康组、模型组大鼠均每日常规腹腔注射生理盐水,CX3CR1干预组向残腔内注射CX3CR1中和抗体进行处理。采用ELISA法检测血清中IL-6、IL-10、IL-1β、TGF-β水平,应用改良X线Norden评分检测骨骼肌微纤维,HE染色观察病理变化,免疫印迹及PCR检测股骨组织中细胞外信号调节蛋白激酶(Extracellular regulated protein kinase,ERK1/2)、丝裂原活化蛋白激酶(Mitogen activated protein kinase,MAPK)蛋白及mRNA表达。结果与健康组比较,模型组TGF-β、IL-1β、IL-10、IL-6等炎症因子含量均升高(P<0.05);与模型组比较,CX3CR1抑制组炎症因子含量降低(P<0.05)。与健康组比较,模型组随时间推移X线Norden评分升高(P<0.05);与模型组比较,CX3CR1抑制组X线Norden评分降低(P<0.05)。HE染色显示,健康组骨质完好;模型组可见大量炎性细胞浸润、灶性脓肿及坏死灶;CX3CR1抑制组大鼠的骨质明显改善,炎症反应降低。与健康组比较,模型组ERK1/2、MAPK蛋白及mRNA表达升高(P<0.05);与模型组比较,CX3CR1抑制组ERK1/2、MAPK蛋白及mRNA表达降低(P<0.05)。结论抑制CX3CR1可改善创伤性骨髓炎大鼠的疾病反应,可能与降低炎症反应、ERK/MAPK信号通路以及改善骨骼肌微纤维相关。Objective To explore the effects of CX3CR1 on inflammatory response,skeletal muscle microfibers and ERK/MAPK signaling pathway in rats with traumatic osteomyelitis.Methods Thirty SPF SD male rats were selected and divided into healthy group,model group and CX3CR1 inhibition group according to random number table method,with an average of 10 in each group.Traumatic osteomyelitis model was established in model group and CX3CR1 inhibition group.The healthy group and model group were routinely injected with normal saline intraperitoneally every day,and the CX3CR1 intervention group was treated by injecting CX3CR1 neutralizing antibody into the residual cavity.Serum levels of inflammatory cytokines interleukin(IL-6,IL-10,IL-1β,TGF-β)were detected by ELISA,skeletal muscle microfibers were detected by X-ray Norden score,and pathological changes were observed by HE staining.Extracellular regulated protein kinase 1/2(ERK1/2),mitogen activated protein kinase(MAPK)protein and mRNA in femur were detected by Western blotting and PCR.Results Compared with the healthy group,the contents of TGF-β,IL-1β,IL-10,IL-6 and other inflammatory factors were increased in the model group(P<0.05).Compared with model group,the content of inflammatory factors in CX3CR1 inhibitory group was decreased(P<0.05).Compared with the healthy group,the X-ray Norden score of the model group was increased over time(P<0.05).Compared with model group,X-ray Norden score of CX3CR1 inhibition group was decreased(P<0.05).HE staining showed that the bone cortex in the healthy group was intact.In the model group,there was a large number of inflammatory cell infiltration,focal abscess,and area necrosis.In the CX3CR1 inhibitory group,the large cortical bone was significantly improved and the inflammatory response was reduced.Compared with healthy group,ERK1/2 and MAPK protein and mRNA in model group were increased(P<0.05).Compared with model group,the protein and mRNA of ERK1/2 and MAPK in CX3CR1 inhibition group were decreased(P<0.05).Conclusion Inhibition of

关 键 词：创伤性骨髓炎 炎症反应 骨骼肌微纤维 细胞外调节蛋白激酶1/2 丝裂原活化蛋白激酶 

分 类 号：R618.2[医药卫生—外科学]