PMID- 36703757
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230202
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 13
DP  - 2022
TI  - The mechanism of oxymatrine on atopic dermatitis in mice based on SOCS1/JAK-STAT3 
      pathway.
PG  - 1091090
LID - 10.3389/fphar.2022.1091090 [doi]
LID - 1091090
AB  - Based on the suppressor of cytokine signaling 1 (SOCS1)/Janus kinase (JAK)/signal 
      transducer and activator of transcription 3 (STAT3) pathway, the mechanism of 
      oxymatrine in the treatment of atopic dermatitis (AD) was preliminarily explored 
      in this study. C57BL/6 mice were induced to establish AD model by smearing 
      carbotriol (MC903) on their back. The AD mice were randomly divided into model 
      group, oxymatrine groups with three dosages (25, 50 and 100 mg/kg), (n = 10). 
      Oxymatrine groups were intragastric administered once daily for 14 days. The same 
      volume of saline was given in the normal control group and model group once daily 
      for 14 days. Subsequently, HE staining was used to observe the pathological 
      changes of skin tissue, ELISA was used to detect the levels of serum inflammatory 
      factors including interleukin-4, 6 and 17 (IL-4, IL-6, and IL-17), tumor necrosis 
      factor-alpha (TNF-alpha) and immunoglobulin E (IgE). Immunohistochemistry was used to 
      detect the expression of suppressor of cytokine signaling 1 and CD3 in skin 
      tissue, and Western blotting was used to detect the proteins in suppressor of 
      cytokine signaling 1/JAK-STAT3 pathway. Compared with the normal control group, 
      the pathological damage of mice in the model group, such as skin hyperplasia, 
      edema, congestion and inflammatory infiltration, aggravated increased 
      significantly. And the expression of serum inflammatory factors, CD3 positive 
      expression and JAK-STAT3 pathway protein in the model group were increased (p < 
      .05), and the expression of suppressor of cytokine signaling 1 protein (p < .05) 
      was decreased. Compared with the model group, the above pathological damage of 
      the mice was reduced, and the serum inflammatory factors, JAK-STAT3 pathway 
      protein, and CD3 positive expression were decreased as a dose-dependant manner (p 
      < .05), and the expression of suppressor of cytokine signaling 1 protein was 
      increased as a dose-dependent manner (p < .05). Oxymatrine can improve the skin 
      inflammation symptoms of AD mice by up regulating the expression of suppressor of 
      cytokine signaling 1, inhibiting the activation of JAK-STAT3 pathway and blocking 
      the activation of T lymphocytes.
CI  - Copyright (c) 2023 Han, Ma, Wang, Jin, Han, Liu and Li.
FAU - Han, Xianwei
AU  - Han X
AD  - Department of Dermatology, The Seventh People's Hospital of Shenyang, Shenyang, 
      China.
FAU - Ma, Tianming
AU  - Ma T
AD  - The Second Hospital of Heilongjiang University of Chinese Medicine, Harbin, 
      China.
FAU - Wang, Qiang
AU  - Wang Q
AD  - Department of Dermatology, The Seventh People's Hospital of Shenyang, Shenyang, 
      China.
FAU - Jin, Chunlin
AU  - Jin C
AD  - Department of Dermatology, The Seventh People's Hospital of Shenyang, Shenyang, 
      China.
FAU - Han, Yusheng
AU  - Han Y
AD  - Heilongjiang University of Chinese Medicine, Harbin, China.
FAU - Liu, Guijun
AU  - Liu G
AD  - Heilongjiang University of Chinese Medicine, Harbin, China.
FAU - Li, Hao
AU  - Li H
AD  - Shenzhen University General Hospital, Shenzhen, China.
LA  - eng
PT  - Journal Article
DEP - 20230110
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC9872557
OTO - NOTNLM
OT  - JAK-STAT3
OT  - SOCS1
OT  - atopic dermatitis
OT  - janus kinase
OT  - oxymatrine
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2023/01/28 06:00
MHDA- 2023/01/28 06:01
PMCR- 2023/01/10
CRDT- 2023/01/27 02:15
PHST- 2022/11/06 00:00 [received]
PHST- 2022/12/14 00:00 [accepted]
PHST- 2023/01/27 02:15 [entrez]
PHST- 2023/01/28 06:00 [pubmed]
PHST- 2023/01/28 06:01 [medline]
PHST- 2023/01/10 00:00 [pmc-release]
AID - 1091090 [pii]
AID - 10.3389/fphar.2022.1091090 [doi]
PST - epublish
SO  - Front Pharmacol. 2023 Jan 10;13:1091090. doi: 10.3389/fphar.2022.1091090. 
      eCollection 2022.