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目的观察川崎病幼兔模型VEGF/PTEN/PI3K信号通路变化,探讨其可能的机制。方法随机将40只幼兔分为正常组(10只)和模型组(30只),模型组按照2.5 ml/kg的剂量,分别于第1天和第14天耳缘静脉注射10%牛血清白蛋白,正常组给予等量0.9%氯化钠溶液注射。分别于造模完成后第1、7、30天收集家兔血清,弓动脉,检测血清白细胞、CK、VEGF水平,HE染色观察各组幼兔弓动脉组织形态学变化,免疫组化染色观察弓动脉PTEN、PI3K表达情况。结果与正常组比较,模型组幼兔,造模后第1天,血清VGEF水平显著升高,表明体内发生炎症反应,而到第7天,VEGF水平呈下降趋势(P<0.01),至第30天,水平恢复至正常幼兔水平。免疫组化结果显示,与正常组比较,在造模后第1天,弓动脉内PTEN表达开始增强,造模后第7、30天,弓动脉内PTEN表达显著增强(P<0.01),而PI3K表达则逐渐减少(P<0.01)。结论 VEGF/PTEN/PI3K信号通路与川崎病的发生、发展有着密切联系。
Objective To observe the changes of VEGF / PTEN / PI3K signaling pathway in Kawasaki disease rabbits and to explore its possible mechanism. Methods A total of 40 rabbits were randomly divided into normal group (n = 10) and model group (n = 30). The model group was treated with 2.5 ml / kg dose of 10% bovine serum on day 1 and day 14 Albumin, normal group given the same amount of 0.9% sodium chloride solution injection. The rabbits’ serum and the arch artery were collected on the 1st, 3rd and 30th day after model establishment, the levels of serum leukocytes, CK and VEGF were measured. The morphological changes of the brains of all rabbits were observed by HE staining and the bows were observed by immunohistochemical staining Artery PTEN, PI3K expression. Results Compared with the normal group, the level of serum VGEF in rabbits in model group was significantly higher than that in the normal group (P <0.01). On the 7th day, the level of VEGF decreased (P <0.01) 30 days, the level returned to the normal level of young rabbits. The results of immunohistochemistry showed that PTEN expression began to increase on the first day after model establishment in the first day after model establishment. PTEN expression was significantly increased (P <0.01) on the 7th and 30th day after modeling PI3K expression was gradually decreased (P <0.01). Conclusion There is a close relationship between VEGF / PTEN / PI3K signaling pathway and the occurrence and development of Kawasaki disease.