TrkA对小鼠过敏性气道反应肺组织Akt/PKB的调节作用

目的 探讨神经生长因子(NGF)受体酪氨酸激酶(TrkA)是否调控丝/苏氨酸激酶(Akt/PKB)磷酸化表达来参与小鼠肺组织过敏性免疫炎性变化。方法 制备卵清蛋白(OVA)致敏的BALB/c小鼠过敏性免疫炎症模型,应用HE肺组织病理染色确定模型成功,采用免疫组织化学、免疫荧光和定量RT-PCR等方法,观察给予TrkA抗体后小鼠肺组织磷酸化Akt(p-Akt)表达变化。结果 p-Akt在过敏性免疫炎症模型小鼠肺组织中表达水平高于正常对照组,TrkA阻断后p-Akt在小鼠肺组织中表达水平明显低于过敏性免疫炎症模型小鼠(p<0.05)。结论 TrkA受体参与NGF介导Akt/PKB传导的小鼠肺部过敏性免疫炎症反应。

The effect of TrkA on the expression of Akt/PKB in mice with airway allergic inflammation

Objective To investigate whether tyrosine kinase（TrkA）, high affinity receptor for the nerve growth factor（NGF） regulates serine/threonine protein kinase（Akt/PKB） phosphorylation to participate in allergic immune inflammatory changes in mice. Methods BALB/c mice were sensitized and challenged with ovalbumin. Pulmonary histological changes were assessed by HE, the effect of TrkA on Akt in allergic airway challenge was assessed by intravenously administering TrkA antibody to the mice. Additionally, phosphorylated Akt （p-Akt） expression was determined by fluorescence microscopy and immunohistochemistry and quantitative RT-PCR. Results The p-Akt overexpression was found in the lungs after allergen challenge by fluorescence microscopy, immuuohistochemistry and RT-PCR, as compared with the control. However, after trealment with anti-TrkA, p-Akt and Akt mRNA levels and allergen-induced airway inflammation were reduced in comparison with those of allergen-challenged mice. Conclusion These results suggest that TrkA regulation of Akt participates in the NGF-mediated development of allergic airway challenge.