Preventative Effects of Antioxidants against PM 10 on Serum IgE Concentration, Mast Cell Counts, Inflammatory Cytokines, and Keratinocyte Differentiation Markers in DNCB-Induced Atopic Dermatitis Mouse Model.
Mi Hee KwackJin Seon BangWeon Ju LeePublished in: Antioxidants (Basel, Switzerland) (2022)
Particulate matter (PM) can cause oxidative stress, inflammation, and skin aging. We investigated the effects of antioxidants such as dieckol, punicalagin, epigallocatechin gallate (EGCG), resveratrol, and Siegesbeckiae Herba extract (SHE) against PM < 10 μm (PM 10 ) on serum IgE concentration, mast cell counts, inflammatory cytokines, and keratinocyte differentiation markers in a 2,4-Dinitrochlorobenzene (DNCB)-induced atopic dermatitis mouse model. Seven-week-old BALB/c mice were sensitized with 2% DNCB. Atopic dermatitis-like lesions were induced on the mice with 0.2% DNCB. Antioxidants and PM 10 were applied to the mice for 4 weeks. PM 10 increased the serum IgE concentration and spleen weight in mice, and all antioxidants downregulated these parameters. Histological examination showed an increase in epidermal thickness and mast cell counts in response to PM 10 , and all antioxidants showed a decrease. PM 10 upregulates the expression of inflammatory cytokines, including interleukin (IL)-1β, IL-4, IL-6, IL-17α, IL-25, IL-31 and thymic stromal lymphopoietin (TSLP) in mice, and all antioxidants inhibited the upregulation of inflammatory cytokines. ELISA showed the same results as real-time PCR. PM 10 downregulates the expression of keratinocyte differentiation markers, including loricrin and filaggrin, in mouse keratinocytes and antioxidants prevented the downregulation of the keratinocyte differentiation markers. Conclusively, PM 10 aggravated the DNCB-induced mouse model in serum IgE concentration, mast cell counts, inflammatory cytokine, and keratinocyte differentiation markers. In addition, antioxidants modulated changes in the DNCB-induced mouse model caused by PM 10 .
Keyphrases
- particulate matter
- air pollution
- atopic dermatitis
- mouse model
- oxidative stress
- diabetic rats
- polycyclic aromatic hydrocarbons
- high glucose
- heavy metals
- poor prognosis
- water soluble
- high fat diet induced
- randomized controlled trial
- type diabetes
- metabolic syndrome
- cell proliferation
- signaling pathway
- peripheral blood
- clinical trial
- bone marrow
- binding protein
- wild type
- heat shock protein
- mass spectrometry
- heat shock
- ischemia reperfusion injury
- double blind