Yagi Sayaka, Tsukatani Toshiaki, Yata Tsuyoshi, Tsukioka Fusae, Miwa Takaki, Furukawa Mitsuru
Department of Otorhinolaryngology, Head and Neck Surgery, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Acta Otolaryngol. 2007 Jul;127(7):748-53. doi: 10.1080/00016480601002062.
Daily intranasal perfusion of lipopolysaccharide (LPS) for 14 days in rats induced apoptosis of olfactory receptor neurons (ORNs) over >3 but <7 days.
Smoking is one of the factors causing olfactory dysfunction. LPS is a major glycolipid component of the gram-negative bacterial cell wall and an active component of cigarette smoke. We studied whether LPS is one of the causes of tobacco-induced olfactory dysfunction by examining apoptosis in the olfactory epithelium after local exposure to LPS.
Rats received intranasal instillation of LPS or saline. Histochemical changes in the olfactory epithelium were examined using antibodies against single-stranded DNA, Bcl-2, Bax, and Caspase-3. We used different concentrations of LPS to examine the dose dependency and observed changes in the olfactory epithelium for a week after exposure cessation to see the duration of the effect of smoking.
We found that numbers of cells positive for ssDNA, Bcl-2, Bax, and Caspase-3 were increased on the exposed side. The number of ssDNA-positive cells reached a maximum on the first day and decreased to normal levels on the seventh day after cessation of exposure.
大鼠连续14天每日经鼻灌注脂多糖（LPS）可在3天以上但不到7天内诱导嗅觉受体神经元（ORN）凋亡。
吸烟是导致嗅觉功能障碍的因素之一。LPS是革兰氏阴性菌细胞壁的主要糖脂成分，也是香烟烟雾的活性成分。我们通过检测局部暴露于LPS后嗅觉上皮细胞的凋亡情况，研究LPS是否为烟草诱导嗅觉功能障碍的原因之一。
给大鼠经鼻滴注LPS或生理盐水。使用抗单链DNA、Bcl-2、Bax和Caspase-3的抗体检测嗅觉上皮的组织化学变化。我们使用不同浓度的LPS来检测剂量依赖性，并在停止暴露后观察嗅觉上皮一周的变化，以了解吸烟影响的持续时间。
我们发现暴露侧单链DNA、Bcl-2、Bax和Caspase-3阳性细胞数量增加。单链DNA阳性细胞数量在暴露第一天达到峰值，并在停止暴露后第七天降至正常水平。
