论文部分内容阅读
目的研究表皮生长因子受体(EGFR)抑制剂C225对宫内感染仔鼠脑组织炎症的影响。方法应用脂多糖(LPS)感染孕鼠建立宫内感染孕鼠模型,给予EGFR抑制剂C225干预,应用免疫组织化学法检测仔鼠脑组织OX42及磷酸化EGFR表达水平的变化,应用酶联免疫吸附测定法(ELISA)检测小胶质细胞活化产物肿瘤坏死因子-α(TNF-α)及白细胞介素-1β(IL-1β)的表达水平。结果与对照组相比,模型组孕鼠所产仔鼠脑组织OX42及磷酸化EGFR的表达明显增强(P<0.01),且TNF-α及IL-1β含量明显增高(P<0.01);与模型组相比,经C225干预后,LPS诱导小胶质细胞活化不明显,OX42及磷酸化EGFR表达明显低于模型组(P<0.01),TNF-α及IL-1β含量也低于模型组(P<0.01)。结论抑制EGFR通路可明显限制LPS诱导的小胶质细胞的激活,EGFR通路可能在外源性感染引起的小胶质细胞活化过程中起桥梁作用,C225可能在神经损伤修复过程中通过调节小胶质细胞起到重要作用。
Objective To investigate the effect of epidermal growth factor receptor (EGFR) inhibitor C225 on brain inflammation in neonatal rats. Methods Pregnant mice infected with lipopolysaccharide (LPS) were intraperitoneally injected with the intraperitoneal injection of C225, and the expression of OX42 and phosphorylated EGFR was detected by immunohistochemical method. The expression of phosphorylated EGFR was detected by enzyme-linked immunosorbent assay The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in microglial cells were detected by ELISA. Results Compared with the control group, the expression of OX42 and phosphorylated EGFR in the pregnant rat model group was significantly increased (P <0.01), and the levels of TNF-α and IL-1β were significantly increased (P <0.01) Compared with model group, the activation of microglial cells induced by LPS was not obvious, the expression of OX42 and phosphorylated EGFR was significantly lower than that of model group (P <0.01), and the content of TNF-α and IL-1β was also lower than that of model group (P <0.01). Conclusion Inhibition of EGFR pathway can significantly inhibit the activation of microglia induced by LPS. EGFR pathway may play a bridging role in microglial activation induced by exogenous infection. C225 may regulate microglia during the process of nerve injury repair Cells play an important role.