“…All reaction experiments were independently repeated three times, and the data were analyzed using the comparison cycle threshold (Ct) method [26]. PCR primers for IL-4 (NM_021283) were 5 -ACC TTG CTG TCA CCC TGT TC-3 (forward), 5 -TTG TGA GCG TGG ACTCAT TC-3 (reverse); TNFα (NM_013693) were 5 -AGC CCC CAG TCT GTA TCC TT-3 (forward) and 5 -CTC CCT TTG CAG AAC TCA GG-3 (reverse); IL-1β (NM_008361) were 5 -CAA CCA ACA AGT GAT ATT CTC CAT G-3 (forward) and 5 -GAT CCA CAC TCT CCA GCT GCA-3 (reverse); IL-25 (NM_080729) were 5 -CAG CAA AGA GCA AGA ACC-3 (forward) and 5 -CCC TGT CCA ACT CAT AGC-3 (reverse); IL-33 (NM_133775) were 5 -CAA TCA GGC GAC GGT GTG GAT GG-3 (forward) and 5 -TCC GGA GGC GAG ACG TCA CC -3 (reverse); for β-actin (NM_007393) were 5 -TCA TCA CCA TCG GCA ACG-3 (forward), 5 -TTC CT GAT GTC CAC GTC GC-3 (reverse) [27]. The mRNA expression was normalized with β-actin and calculated based on the ratio to 100% of the phorbol 12-myristate 13-acetate (PMA)/ionomycin-treated group, the oxazolone-treated group or DNCB-treated group.…”
Section: Determination Of Gene Expressionmentioning
To investigate the potential effects of acorn shells on atopic dermatitis (AD), we utilized oxazolone (OX)-or 2,4-dinitrochlorobenzene (DNCB)-induced AD-like lesion mouse models. Our research demonstrates that Acorn shell extract (ASE) improved the progression of AD-like lesions, including swelling, which were induced by oxazolone on Balb/c mouse ears. Additionally, ASE significantly decreased the ear thickness (OX: 0.42 ± 0.01 mm, OX-ASE: 0.32 ± 0.02 mm) and epidermal thickness (OX: 75.3 ± 32.6 µm, OX-ASE: 46.1 ± 13.4 µm). The continuous DNCB-induced AD mouse model in SKH-1 hairless mice demonstrated that ASE improved AD-like symptoms, including the recovery of skin barrier dysfunction, Immunoglobulin E hyperproduction (DNCB: 340.1 ± 66.8 ng/mL, DNCB-ASE: 234.8 ± 32.9 ng/mL) and an increase in epidermal thickness (DNCB: 96.4 ± 21.9 µm, DNCB-ASE: 52.4 ± 16.3 µm). In addition, we found that ASE suppressed the levels of AD-involved cytokines, such as Tumor Necrosis Factor α, IL-1β, IL-25 and IL-33 in both animal models. Furthermore, gallic acid and ellagic acid isolated from ASE suppressed β-hexosaminidase release and IL-4 expression in RBL-2H3 cells. The acorn shell and its active phytochemicals have potential as a new remedy for the improvement of atopic dermatitis and other inflammatory diseases.
“…All reaction experiments were independently repeated three times, and the data were analyzed using the comparison cycle threshold (Ct) method [26]. PCR primers for IL-4 (NM_021283) were 5 -ACC TTG CTG TCA CCC TGT TC-3 (forward), 5 -TTG TGA GCG TGG ACTCAT TC-3 (reverse); TNFα (NM_013693) were 5 -AGC CCC CAG TCT GTA TCC TT-3 (forward) and 5 -CTC CCT TTG CAG AAC TCA GG-3 (reverse); IL-1β (NM_008361) were 5 -CAA CCA ACA AGT GAT ATT CTC CAT G-3 (forward) and 5 -GAT CCA CAC TCT CCA GCT GCA-3 (reverse); IL-25 (NM_080729) were 5 -CAG CAA AGA GCA AGA ACC-3 (forward) and 5 -CCC TGT CCA ACT CAT AGC-3 (reverse); IL-33 (NM_133775) were 5 -CAA TCA GGC GAC GGT GTG GAT GG-3 (forward) and 5 -TCC GGA GGC GAG ACG TCA CC -3 (reverse); for β-actin (NM_007393) were 5 -TCA TCA CCA TCG GCA ACG-3 (forward), 5 -TTC CT GAT GTC CAC GTC GC-3 (reverse) [27]. The mRNA expression was normalized with β-actin and calculated based on the ratio to 100% of the phorbol 12-myristate 13-acetate (PMA)/ionomycin-treated group, the oxazolone-treated group or DNCB-treated group.…”
Section: Determination Of Gene Expressionmentioning
To investigate the potential effects of acorn shells on atopic dermatitis (AD), we utilized oxazolone (OX)-or 2,4-dinitrochlorobenzene (DNCB)-induced AD-like lesion mouse models. Our research demonstrates that Acorn shell extract (ASE) improved the progression of AD-like lesions, including swelling, which were induced by oxazolone on Balb/c mouse ears. Additionally, ASE significantly decreased the ear thickness (OX: 0.42 ± 0.01 mm, OX-ASE: 0.32 ± 0.02 mm) and epidermal thickness (OX: 75.3 ± 32.6 µm, OX-ASE: 46.1 ± 13.4 µm). The continuous DNCB-induced AD mouse model in SKH-1 hairless mice demonstrated that ASE improved AD-like symptoms, including the recovery of skin barrier dysfunction, Immunoglobulin E hyperproduction (DNCB: 340.1 ± 66.8 ng/mL, DNCB-ASE: 234.8 ± 32.9 ng/mL) and an increase in epidermal thickness (DNCB: 96.4 ± 21.9 µm, DNCB-ASE: 52.4 ± 16.3 µm). In addition, we found that ASE suppressed the levels of AD-involved cytokines, such as Tumor Necrosis Factor α, IL-1β, IL-25 and IL-33 in both animal models. Furthermore, gallic acid and ellagic acid isolated from ASE suppressed β-hexosaminidase release and IL-4 expression in RBL-2H3 cells. The acorn shell and its active phytochemicals have potential as a new remedy for the improvement of atopic dermatitis and other inflammatory diseases.
“…Infusions of génépi group plants has long been used as thermogenic agents to fatigue, indigestion, and airway infections in people . Modern medical research has revealed the pharmacological effects of eupatilin on anti‐inflammatory, anti‐ulcer, anti‐oxidative, and antineoplastic agent . In addition, eupatilin has shown anti‐diabetic, anti‐arthritis, and anti‐proliferative activity.…”
Eupatilin (5,7-dihydroxy-3 0 ,4 0 ,6-trimethoxyflavone) is a natural active substance found in génépi group plants, and its pharmacological activities has been proven to be useful in the treatment of various cancers. However, whether eupatilin demonstrates anti-cancer activity in cervical cancer is still under evaluation. To clarify this, cancer cell lines and nude mouse model were used in this study. The results indicated that eupatilin could inhibit the occurrence of cervical cancer both in vivo and in vitro.Cervical cancer cell lines (C4-1, HeLa, Caski, and Siha) and Ect1/E6E7 cells were incubated with eupatilin (40μM) for 48 hours. Compared with the control group, the viability of cervical cancer cells decreased significantly, while the apoptotic cells increased significantly. Cell cycle analysis showed that eupatilin treatment of HeLa and Caski cells reduced the proliferation index. Eupatilin at 40 mg/kg also inhibited tumour growth in tumour-bearing mice. Interestingly, weakened hedgehog signalling was observed in cervical cancer cells and tumours from tumour-bearing mice after eupatilin treatment. Our results reveal the inhibitory effect of eupatilin on cervical cancer and shed new light on the molecular mechanism of its therapeutic effect.
“…Furthermore, PM can penetrate the skin through hair follicles and cause epidermal thickening and dermal inflammation in disrupted skin 17,18 . AD is a chronic relapsing inflammatory skin disease characterized by complex interactions among genetic predisposition, environmental factors, immune dysregulation, and skin barrier dysfunction [19][20][21][22] . Recently, several epidemiologic studies have investigated the effects of PM in patients with AD 1,[22][23][24][25][26] .…”
Section: Introductionmentioning
confidence: 99%
“…AD is a chronic relapsing inflammatory skin disease characterized by complex interactions among genetic predisposition, environmental factors, immune dysregulation, and skin barrier dysfunction [19][20][21][22] . Recently, several epidemiologic studies have investigated the effects of PM in patients with AD 1,[22][23][24][25][26] . However, the results of these studies are controversial: several studies demonstrated that ambient PM is related to the exacerbation of AD symptoms [22][23][24]27 ; in contrast, others report that AD is not related to urbanization and industrialization 25,26 .…”
Background
Recent epidemiological studies have demonstrated that air pollution is associated with the inflammatory response and may aggravate inflammatory skin diseases such as atopic dermatitis (AD). However, it is unclear whether particulate matter (PM) aggravates AD symptoms.
Objective
The aim of this study was to investigate whether PM exposure affects the skin barrier dysfunction and aggravates AD symptoms using human keratinocytes (HaCaT) cells and a mouse model of oxazolone-induced AD-like skin.
Methods
Standard reference material (SRM) 1649b, which mainly comprises polycyclic aromatic hydrocarbons, was used as the reference PM. HaCaT cells and mouse model of oxazolone-induced AD-like skin were treated with PM. The mRNA or protein expression levels of stratum corneum (SC) and tight junction (TJ) proteins, inflammatory cytokines, as well as clinical and histological changes of the AD-like skin of mouse model were evaluated. The expression of genes and proteins was analyzed by real-time polymerase chain reaction and Western blotting. Levels of inflammatory cytokines were measured by enzyme-linked immunosorbent assay.
Results
The results revealed that PM downregulates the expression levels of several SC and TJ-related proteins in the mouse model with AD-like skin. Clinically, epidermal and dermal thickness was significantly increased and dermal inflammation was prominent in PM treated AD-like skin.
Conclusion
In conclusion, we found that PM aggravates skin barrier dysfunction, clinically augmenting epidermal and dermal thickening with dermal inflammation in AD-like skin. These results suggest that PM may trigger the exacerbation of AD symptoms via skin barrier dysfunction-related mechanisms.
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