PMID- 33911646
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220422
IS  - 2005-3894 (Electronic)
IS  - 1013-9087 (Print)
IS  - 1013-9087 (Linking)
VI  - 31
IP  - 5
DP  - 2019 Oct
TI  - Therapeutic Effect of Glucosamine on an Atopic Dermatitis Animal Model.
PG  - 538-544
LID - 10.5021/ad.2019.31.5.538 [doi]
AB  - BACKGROUND: 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-kappaB pathway. OBJECTIVE: We aimed to investigate the effect of GlcN 
      on atopic dermatitis (AD) in an animal model. METHODS: 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. RESULTS: Clinical dermatitis scores decreased 
      with increasing GlcN dose (p<0.001). Concentrations of tissue IL-13 and IL-17 
      decreased after GlcN administration (each group: p=0.002 and p<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 
      (p=0.004). Histopathological scores were not significantly different among groups 
      B~E (p=0.394). CONCLUSION: GlcN improved AD symptoms and decreased tissue IL-13, 
      IL-17, and serum total IgE levels in an animal model.
CI  - Copyright (c) 2019 The Korean Dermatological Association and The Korean Society for 
      Investigative Dermatology.
FAU - Yoon, Hee Seong
AU  - Yoon HS
AUID- ORCID: 0000-0001-8997-9697
AD  - Department of Dermatology, Inha University School of Medicine, Incheon, Korea.
FAU - Byun, Ji Won
AU  - Byun JW
AUID- ORCID: 0000-0003-0317-6725
AD  - Department of Dermatology, Inha University School of Medicine, Incheon, Korea.
FAU - Shin, Jeonghyun
AU  - Shin J
AUID- ORCID: 0000-0002-4995-9533
AD  - Department of Dermatology, Inha University School of Medicine, Incheon, Korea.
FAU - Kim, Young Hyo
AU  - Kim YH
AUID- ORCID: 0000-0002-3623-1770
AD  - Department of Otorhinolaryngology-Head and Neck Surgery, Inha University School 
      of Medicine, Incheon, Korea.
FAU - Choi, Gwang Seong
AU  - Choi GS
AUID- ORCID: 0000-0002-5766-0179
AD  - Department of Dermatology, Inha University School of Medicine, Incheon, Korea.
LA  - eng
PT  - Journal Article
DEP - 20190830
PL  - Korea (South)
TA  - Ann Dermatol
JT  - Annals of dermatology
JID - 8916577
PMC - PMC7992559
OTO - NOTNLM
OT  - Allergy and immunology
OT  - Anti-allergic agents
OT  - Atopic dermatitis
OT  - Glucosamine
COIS- CONFLICTS OF INTEREST: The authors have nothing to disclose.
EDAT- 2019/10/01 00:00
MHDA- 2019/10/01 00:01
PMCR- 2019/10/01
CRDT- 2021/04/29 06:21
PHST- 2019/05/30 00:00 [received]
PHST- 2019/07/01 00:00 [revised]
PHST- 2019/07/05 00:00 [accepted]
PHST- 2021/04/29 06:21 [entrez]
PHST- 2019/10/01 00:00 [pubmed]
PHST- 2019/10/01 00:01 [medline]
PHST- 2019/10/01 00:00 [pmc-release]
AID - 10.5021/ad.2019.31.5.538 [doi]
PST - ppublish
SO  - Ann Dermatol. 2019 Oct;31(5):538-544. doi: 10.5021/ad.2019.31.5.538. Epub 2019 
      Aug 30.