核因子-κBp65、缺氧诱导因子-1α及血管内皮生长因子在变应性鼻炎小鼠鼻黏膜中的表达

Expression of nuclear factor-κB p65, hypoxia inducible factor 1α and vascular endothelial growth factor in the nasal mucosa of allergic rhinitis mice

目的探讨核因子-κB p65(nuclear factor-κBp65,NF-κB p65)、缺氧诱导因子-1α(hypoxia induciblefactor 1α,HIF-1α)及血管内皮生长因子(vascularendothelial growth factor,VEGF)在变应性鼻炎(AR)小鼠鼻黏膜中的表达及其相关性研究。方法 30只FVB系小鼠随机分为对照组、AR组及激素干预组,AR组采用腹腔注射卵清蛋白(ovalbumin,OVA)致敏,滴鼻局部激发OVA悬液制备模型。对照组以生理盐水代替OVA,激素干预组每次激发前地塞米松腹腔注射干预。鼻黏膜采用HE染色和免疫组化染色,观察形态学改变和NF-κBp65、HIF-1α及VEGF的表达情况。结果 NF-κB p65、HIF-1α及VEGF在小鼠鼻黏膜的表达是一致的,AR组均较对照组和激素干预组显著增加,差异有显著性(F分别为13.22、16.79、11.84,P均<0.05)。经相关性分析,在AR组中,NF-κBp65与HIF-1α的表达呈正相(r=0.655,P<0.05),HIF-1α与VEGF的表达也呈正相关(r=0.698,P<0.05)。结论在炎症、低氧等刺激下,活化的NF-κB p65通过调控HIF-1α的表达上调VEGF的表达,促进小鼠过敏性气道炎症的发生。

OBJECTIVE To investigate the expression and correlation among nuclear factor-kB p65 （NF-kB p65） , hypoxia inducible factor 1a （HIF-1a） and vascular endothelial growth factor （VEGF） in the nasal mucosa of allergic rhinitis mice. METHODS Thirty FVB mice were randomly divided into control group, allergic rhinitis group （AR group） and hormone intervention group. AR group conducted the basal sensitization with intraperitoneal injection of egg albumin （ovalbumin, OVA） , and then exposed to OVA suspension intranasally, so as to induce mouse model of allergic rhinitis. Saline was used in control group instead of OVA, Hormone intervention group conducted intraperitoneal injection of dexamethasone before local excitation. The nasal tissues ere stained with hematoxlin-eosin for histological analysis and immunohistochemical staining for the expression of NF-KB p65, HIF-1a and VEGF. RESULTS Compared with the control group and intervention group, the expression of NF-KB p65, HIF-1a and VEGF in AR group were significantly higher, and the differences were significant（the values of F were 13.22, 16.79 and 11.84, P〈0.05）. There was positive correlation between HIF- 1a and NF-KB in nasal mucosa of AR group （P〈0.05） , here was also positive correlation between HIF-1a and VEGF in nasal mucosa of AR group （P〈0.05） . CONCLUSION The results suggested that under the stimulation such as inflammation and low oxygen, p65 regulates the expression of the HIF-1a, which promotes the expression of VEGF in mice, that make the allergic airway inflammation occurred.