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The Impact of Ovariectomy on Olfactory Neuron Regeneration in Mice.
Chemical Senses ( IF 2.8 ) Pub Date : 2020-04-17 , DOI: 10.1093/chemse/bjaa005
Kentaro Yamada 1 , Hideaki Shiga 1 , Takuya Noda 1 , Masayuki Harita 1 , Tomoko Ishikura 1 , Yukari Nakamura 1 , Toshihisa Hatta 2 , Hiromi Sakata-Haga 2 , Hiroki Shimada 2 , Takaki Miwa 1
Affiliation  

Estrogen has been shown to affect differentiation and proliferation as a mitogen in various neural systems. Olfactory receptor cells are unique within the nervous system, and have the ability to regenerate even after an individual has reached maturity. Olfactory receptor cells also regenerate after experimentally induced degeneration. The purpose of this study is to observe the influence of estrogen depletion induced by ovariectomy on olfactory nerve regeneration. Female mice underwent bilateral ovariectomy at 8 weeks of age and received intraperitoneal administration of methimazole 1 week later. At 2, 4, and 6 weeks after methimazole administration, the olfactory mucosa was analyzed histochemically to determine olfactory epithelium (OE) thickness, olfactory marker protein distribution, and Ki-67 immunoreactivity. Furthermore, 2 weeks after ovariectomy, trkA protein distribution in the OE and nerve growth factor (NGF) levels in the olfactory bulb were determined by immunohistochemistry and enzyme-linked immunosorbent assay, respectively. Our results showed that in ovariectomized mice OMP, Ki-67, and trkA-immunopositive cells expression decreased at 2 weeks after methimazole injection, a time point at which regeneration is underway. At this same time point, although NGF production in the olfactory bulb had increased before methimazole administration, no differences were observed between the ovx and control groups. These results suggest that estrogen depletion induces a suppressive effect on regeneration of olfactory neurons, and that estrogen may have a potential use in the treatment of sensorineural olfactory dysfunction.

中文翻译:

卵巢切除术对小鼠嗅觉神经元再生的影响。

雌激素已显示出在各种神经系统中作为有丝分裂原影响分化和增殖。嗅觉受体细胞在神经系统中是独特的,即使个体成熟后也具有再生能力。嗅觉受体细胞在实验诱导的变性后也会再生。这项研究的目的是观察卵巢切除术引起的雌激素耗竭对嗅觉神经再生的影响。雌性小鼠在8周大时进行双侧卵巢切除术,并在1周后接受腹膜内给予他巴唑。甲巯咪唑给药后第2、4和6周,组织化学分析嗅觉粘膜,以确定嗅觉上皮(OE)厚度,嗅觉标记蛋白分布和Ki-67免疫反应性。此外,卵巢切除术后2周,分别通过免疫组织化学和酶联免疫吸附法测定OE中的trkA蛋白分布和嗅球中的神经生长因子(NGF)水平。我们的研究结果表明,在去甲卵巢小鼠中,注射甲他咪唑2周后OMP,Ki-67和trkA免疫阳性细胞表达下降,此时再生正在进行。在同一时间点,尽管在服用甲巯咪唑之前嗅球中的NGF产量增加了,但在ovx和对照组之间未观察到差异。这些结果表明,雌激素的消耗对嗅觉神经元的再生具有抑制作用,并且雌激素可能在治疗感觉神经嗅觉功能障碍中具有潜在用途。分别通过免疫组织化学和酶联免疫吸附法测定了trkA蛋白在OE中的分布和嗅球中神经生长因子(NGF)的水平。我们的研究结果表明,在去甲卵巢小鼠中,注射甲他咪唑2周后OMP,Ki-67和trkA免疫阳性细胞表达下降,此时再生正在进行。在同一时间点,尽管在服用甲巯咪唑之前嗅球中的NGF产量增加了,但在ovx和对照组之间未观察到差异。这些结果表明,雌激素的消耗对嗅觉神经元的再生具有抑制作用,并且雌激素可能在治疗感觉神经嗅觉功能障碍中具有潜在用途。分别通过免疫组织化学和酶联免疫吸附法测定了trkA蛋白在OE中的分布和嗅球中神经生长因子(NGF)的水平。我们的研究结果表明,在去甲卵巢小鼠中,注射甲他咪唑2周后OMP,Ki-67和trkA免疫阳性细胞表达下降,此时再生正在进行。在同一时间点,尽管在服用甲巯咪唑之前嗅球中的NGF产量增加了,但在ovx和对照组之间未观察到差异。这些结果表明,雌激素的消耗对嗅觉神经元的再生具有抑制作用,并且雌激素可能在治疗感觉神经嗅觉功能障碍中具有潜在用途。
更新日期:2020-04-18
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