Age-related olfactory dysfunction: cellular and molecular analyses

1. 热量限制加剧了小鼠嗅觉黏膜的年龄相关性神经上皮变性，也加剧了损伤后嗅觉神经上皮的再生。热量限制对神经上皮细胞增殖活性的下调似乎在发病机制中起重要作用。2. 利用合成的病毒双链RNA类似物Poly（I:C）建立了小鼠病毒后嗅觉障碍（PVOD）免疫模型。这些分析表明，中性粒细胞介导的先天免疫反应引起的继发性损伤在PVOD的发病机制中起重要作用。3. 对雌激素受体（ERbeta）缺失小鼠的分析表明，雌激素通过ERbeta参与嗅粘膜的内稳态。4. FAT-1小鼠在损伤后表现出更好的神经上皮再生，提示组织脂肪酸与嗅觉神经上皮再生有关。

1. Caloric restriction exacerbated the age-related neuroepithelial degeneration in the mouse olfactory mucosa and also worsened the regeneration of the olfactory neuroepithelium after injury. The downregulation of proliferative activity in neuroepithelium by caloric restriction appeared to play an important role in the pathogenesis. 2. The immune model of postviral olfactory disorder (PVOD) was developed in mice using Poly(I:C), a synthetic analog of viral double-stranded RNA. The analyses suggested that the secondary damage caused by the neutrophil-mediated innate immune response plays an important role in the pathogenesis of PVOD. 3. The analyses of estrogen receptor beta (ERbeta) -deficient mice suggested that estrogen plays a role in the homeostasis of the olfactory mucosa through ERbeta. 4. FAT-1 mice demonstrated better neuroepithelical regeneration after injury, suggesting that the tissue fatty acid is associated with the regeneration of the olfactory neuroepithelium.