Effect of ginkgo biloba and dexamethasone in the treatment of 3-methylindole-induced anosmia mouse model.

Chul Hee Lee, Ji-Hun Mo, Seung Hee Shim, Jung-Min Ahn, Jeong-Whun Kim
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引用次数: 15

Abstract

Background: Olfactory loss is a challenging disease. Although glucocorticoid is sometimes used for the treatment of anosmia, it has been reported that it potentiated neural damage in the early phase of treatment. This study is designed to identify the effect of ginkgo biloba, an antioxidant that acts as a free radical scavenger, in the treatment of olfactory injury aggravated by dexamethasone.

Methods: Anosmia mouse model was induced by i.p. injection of 3-methylindole (3-MI). Twenty-five mice were divided into one control group without anosmia and four anosmia treatment groups (given treatments of dexamethasone and/or ginkgo biloba). The effects of treatment were evaluated by behavioral test, Western blot, and immunohistochemistry 2 weeks after 3-MI injection.

Results: Induction of anosmia was confirmed by behavioral tests. The thickness and cell number of olfactory neuroepithelium were decreased more significantly in the dexamethasone treatment group than in the combination treatment group. The expression of olfactory marker protein (OMP) in olfactory epithelium was more decreased also in the dexamethasone treatment group than in the combination treatment group. The expression of OMP was decreased significantly in the olfactory bulbs of anosmia groups but there were no differences between the anosmia treatment groups.

Conclusion: Dexamethasone treatment was associated with further deterioration of olfactory injury by 3-MI and it was recovered by combination treatment of dexamethasone and ginkgo biloba. The antioxidant effect of ginkgo biloba might play a role in restoration of olfactory loss and it was effective only when oxidative stress is maximized by dexamethasone.

银杏叶和地塞米松对3-甲基林多致嗅觉缺失小鼠模型的治疗作用。
背景:嗅觉丧失是一种具有挑战性的疾病。虽然糖皮质激素有时用于治疗嗅觉缺失,但据报道,它在治疗的早期阶段会加剧神经损伤。本研究旨在确定银杏叶,一种具有自由基清除作用的抗氧化剂,在治疗地塞米松加重的嗅觉损伤中的作用。方法:采用腹腔注射3-甲基吲哚(3-MI)建立小鼠嗅觉缺失模型。将25只小鼠分为无嗅觉缺失对照组和4个嗅觉缺失治疗组(给予地塞米松和/或银杏叶治疗)。注射3-MI 2周后,通过行为测试、免疫印迹和免疫组化评价治疗效果。结果:通过行为测试证实了嗅觉缺失的诱导。地塞米松治疗组嗅神经上皮细胞厚度和细胞数量明显低于联合治疗组。地塞米松治疗组大鼠嗅上皮嗅觉标记蛋白(OMP)表达明显低于联合治疗组。嗅觉缺失组嗅球中OMP的表达明显降低,但嗅觉缺失治疗组间无差异。结论:地塞米松治疗与3-MI嗅觉损伤的进一步恶化有关,地塞米松联合银杏叶可使其恢复。银杏叶的抗氧化作用可能对嗅觉丧失的恢复有一定的作用,只有在地塞米松使氧化应激最大化的情况下才有效。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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