PMID- 37439364
OWN - NLM
STAT- MEDLINE
DCOM- 20231003
LR  - 20231005
IS  - 1440-1681 (Electronic)
IS  - 0305-1870 (Linking)
VI  - 50
IP  - 11
DP  - 2023 Nov
TI  - Esculentoside A ameliorates DNCB-induced atopic dermatitis by suppressing the 
      ROS-NLRP3 axis via activating the Nrf2 pathway.
PG  - 844-854
LID - 10.1111/1440-1681.13809 [doi]
AB  - Atopic dermatitis (AD) is a chronic inflammatory skin condition with a high 
      prevalence. Inflammation and oxidative stress are strongly associated with AD 
      progression. Esculentoside A (EsA) inhibits inflammation and oxidative stress in 
      various diseases. However, whether EsA mitigates AD by suppressing inflammation 
      and oxidative stress remains unknown. A mouse model of AD was constructed by the 
      induction of 1-chloro-2,4-dinitrochlorobenzene (DNCB). The mechanism of EsA and 
      its effects on AD symptoms, pathology, inflammation and oxidative stress were 
      investigated through histopathological staining, enzyme-linked immunosorbent 
      assay, blood cells analysis, colorimetric measurement and western blot analysis. 
      EsA improved the clinical symptoms and increased clinical skin scores in AD mice. 
      Skin thickening of the epidermis and dermal tissues and the mast cell numbers in 
      AD mice were reduced with the EsA treatment. EsA decreased the relative mRNA 
      level of thymic stromal lymphopoietin, interleukin (IL)-4, IL-5 and IL-13; the 
      serum concentrations of immunoglobulin E (IgE) and IL-6; and the numbers of white 
      blood cells (WBC) and WBC subtypes, including basophil, lymphocytes, eosinophil, 
      neutrophil and monocytes in DNCB-induced mice. DNCB caused higher levels of 
      oxidative stress, which was reversed with the administration of EsA. 
      Mechanically, EsA upregulated the expression of Nrf2 but downregulated the level 
      of NLRP3 inflammasome in AD mice. The inhibitor of Nrf2 significantly recovered 
      the EsA-induced changes in the NLRP3 inflammasome proteins in DNCB-treated mice. 
      Therefore, EsA improved the clinical and pathological symptoms, inflammation and 
      oxidative stress experienced by DNCB-induced mice and was involved in the 
      inactivation of NLRP3 inflammasome by activating Nrf2.
CI  - (c) 2023 John Wiley & Sons Australia, Ltd.
FAU - Liu, Tao
AU  - Liu T
AD  - Department of Dermatology, Affiliated Hospital of Southwest Medical University, 
      Luzhou, China.
FAU - He, Yuanmin
AU  - He Y
AD  - Department of Dermatology, Affiliated Hospital of Southwest Medical University, 
      Luzhou, China.
FAU - Liao, Yongmei
AU  - Liao Y
AD  - Department of Dermatology, Affiliated Hospital of Southwest Medical University, 
      Luzhou, China.
LA  - eng
PT  - Journal Article
DEP - 20230713
PL  - Australia
TA  - Clin Exp Pharmacol Physiol
JT  - Clinical and experimental pharmacology & physiology
JID - 0425076
RN  - 0 (Dinitrochlorobenzene)
RN  - 65497-07-6 (esculentoside A)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Inflammasomes)
RN  - 0 (Cytokines)
SB  - IM
MH  - Animals
MH  - Mice
MH  - *Dermatitis, Atopic/chemically induced/drug therapy
MH  - Dinitrochlorobenzene/toxicity/metabolism
MH  - NF-E2-Related Factor 2/metabolism
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Inflammasomes/metabolism
MH  - Skin
MH  - Cytokines/metabolism
MH  - Inflammation/metabolism
MH  - Mice, Inbred BALB C
OTO - NOTNLM
OT  - Esculentoside A
OT  - NLRP3
OT  - Nrf2
OT  - atopic dermatitis
OT  - inflammation
OT  - oxidative stress
EDAT- 2023/07/13 12:31
MHDA- 2023/10/03 06:47
CRDT- 2023/07/13 06:41
PHST- 2023/06/13 00:00 [revised]
PHST- 2023/04/12 00:00 [received]
PHST- 2023/06/19 00:00 [accepted]
PHST- 2023/10/03 06:47 [medline]
PHST- 2023/07/13 12:31 [pubmed]
PHST- 2023/07/13 06:41 [entrez]
AID - 10.1111/1440-1681.13809 [doi]
PST - ppublish
SO  - Clin Exp Pharmacol Physiol. 2023 Nov;50(11):844-854. doi: 
      10.1111/1440-1681.13809. Epub 2023 Jul 13.