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目的探讨鼻腔吸入IFN-γ对大鼠变应性鼻炎(AR)的治疗作用及其机制。方法将32只大鼠随机分为四组,各8只。A组为阴性对照组。B、C、D组采用卵清蛋白、氢氧化铝建立大鼠AR模型,B组为阳性对照组、C组为IFN-γ治疗组、D组为丙酸倍氯米松治疗对照组。B、C、D组于模型建立后第31～38天,每只每日每侧鼻腔分别滴入PBS50μl、IFN-γ1μg和丙酸倍氯米松3.5μg。第39天取鼻腔黏膜,观察鼻腔组织病理学改变,用免疫组化SP法检测转录因子GATA3。结果与A组相比,B组鼻黏膜充血、水肿,黏膜层增厚,有嗜酸细胞为主的炎性细胞浸润,GATA3表达增加;C、D组上述炎性改变明显减轻,鼻黏膜中GATA3表达减少。结论鼻腔滴入IFN-γ治疗AR可能与阻断GATA3表达,从而继发抑制Th2型反应有关。
Objective To investigate the therapeutic effect of nasal inhalation of IFN-γ on allergic rhinitis (AR) in rats and its mechanism. Methods Thirty-two rats were randomly divided into four groups with 8 rats each. A group was negative control group. Group B, C and D used ovalbumin and aluminum hydroxide to establish AR model in rats. Group B was positive control group, group C was IFN-γ treatment group and group D was beclometasone dipropionate treatment control group. Groups B, C and D were injected with 50μl of PBS, IFN-γ1μg and 3.5μg of beclomethasone propionate respectively on the nasal cavity on the 31st day to the 38th day after model establishment. Nasal mucosa was taken on the 39th day to observe the pathological changes of the nasal tissue. The transcription factor GATA3 was detected by immunohistochemical SP method. Results Compared with group A, the nasal mucosa in group B had hyperemia, edema, thickening of mucosa, eosinophilic inflammatory cell infiltration and increased GATA3 expression. The inflammatory changes in group C and group D were significantly reduced. In group B, GATA3 expression decreased. Conclusion Nasal instillation of IFN-γ in the treatment of AR may be related to blocking the expression of GATA3 and consequently inhibiting the Th2-type response.