Yoon Hee Seong, Byun Ji Won, Shin Jeonghyun, Kim Young Hyo, Choi Gwang Seong
Department of Dermatology, Inha University School of Medicine, Incheon, Korea.
Department of Otorhinolaryngology-Head and Neck Surgery, Inha University School of Medicine, Incheon, Korea.
Ann Dermatol. 2019 Oct;31(5):538-544. doi: 10.5021/ad.2019.31.5.538. Epub 2019 Aug 30.
Recent studies have reported that glucosamine (GlcN) showed therapeutic effects in allergic diseases such as asthma and rhinitis, and its mechanisms include the suppression of T helper type 2 immune responses and the nuclear factor-κB pathway.
We aimed to investigate the effect of GlcN on atopic dermatitis (AD) in an animal model.
Twenty-five BALB/c mice were divided into five groups (groups A~E). Group A was the phosphate-buffered saline (PBS)-treated group without AD induction. Group B was the PBS control group with AD induction. Groups C to E were the AD induction groups, which were treated with three different doses of GlcN (10 mg, 20 mg, and 40 mg, respectively). Histopathological examination was performed after GlcN administration. Interleukin (IL)-4, IL-13, and IL-17 cytokine levels were measured by enzyme-linked immunosorbent assay using skin biopsy specimens. Serum total immunoglobulin E (IgE) concentrations were measured before and after administration with GlcN or PBS.
Clinical dermatitis scores decreased with increasing GlcN dose (<0.001). Concentrations of tissue IL-13 and IL-17 decreased after GlcN administration (each group: =0.002 and <0.001, respectively), but the concentrations of tissue IL-4 did not show differences across groups. Serum IgE levels tended to be lower after GlcN administration (=0.004). Histopathological scores were not significantly different among groups B~E (=0.394).
GlcN improved AD symptoms and decreased tissue IL-13, IL-17, and serum total IgE levels in an animal model.
最近的研究报道，氨基葡萄糖（GlcN）在哮喘和鼻炎等过敏性疾病中显示出治疗作用，其机制包括抑制2型辅助性T细胞免疫反应和核因子-κB途径。
我们旨在研究GlcN在动物模型中对特应性皮炎（AD）的影响。
将25只BALB/c小鼠分为五组（A~E组）。A组为未诱导AD的磷酸盐缓冲盐水（PBS）处理组。B组为诱导AD的PBS对照组。C至E组为AD诱导组，分别用三种不同剂量的GlcN（分别为10 mg、20 mg和40 mg）进行治疗。给予GlcN后进行组织病理学检查。使用皮肤活检标本通过酶联免疫吸附测定法测量白细胞介素（IL）-4、IL-13和IL-17细胞因子水平。在给予GlcN或PBS前后测量血清总免疫球蛋白E（IgE）浓度。
随着GlcN剂量增加，临床皮炎评分降低（<0.001）。给予GlcN后，组织IL-13和IL-17浓度降低（每组分别为=0.002和<0.001），但组织IL-4浓度在各组间未显示差异。给予GlcN后血清IgE水平趋于降低（=0.004）。B至E组之间的组织病理学评分无显著差异（=0.394）。
在动物模型中，GlcN改善了AD症状，并降低了组织IL-13、IL-17和血清总IgE水平。
