组织工程与重建外科杂志

组织工程与重建外科杂志 ›› 2024, Vol. 20 ›› Issue (1): 58-.

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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

  

  • 发布日期:2024-03-07

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

  • Published:2024-03-07

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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。

关键词:

Abstract:

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 ofERK1/2 and MAPK in CX3CR1 inhibition group were decreased （P<0.05）. Conclusion Inhibition of CX3CR1 can improvethe disease response in traumatic osteomyelitis rats， which may be related to decreased inflammatory response， ERK/MAPK
and improved skeletal muscle microfibers

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