Angelica Yinzi alleviates 1-chloro-2,4-dinitrobenzene-induced atopic dermatitis by inhibiting activation of NLRP3 inflammasome and down-regulating the MAPKs/NF-kB signaling pathway

Liu, Wei; Song, Wook; Luo, Yadong; Dan, Hanxiong; Li, Li; Zhang, Zhouyang; Zhou, Daonian; Peng, You

doi:10.1016/j.jsps.2022.07.003

Cited by 11 publications

(10 citation statements)

References 44 publications

(39 reference statements)

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“…42 Many studies have proven that suppressing NLRP3 inflammasome contributes to the mitigation of AD. [64][65][66] In the present study, the expression of Nrf2 was increased, and that of NLRP3 inflammasomerelated proteins was decreased in dorsal skin tissues from DNCBinduced mice, indicating the activation of Nrf2 signalling and inactivation of NLRP3 inflammasome in AD mice, coinciding with previous results. 64 However, the treatment of EsA further enhanced the Nrf2 expression but reduced the level of NLRP3 inflammasome in DNCBinduced mice.…”

Section: Discussionsupporting

confidence: 92%

“…NLRP3 inflammasome plays a vital role in the development of AD, and the activation of NLRP3 inflammasome induces AD 42 . Many studies have proven that suppressing NLRP3 inflammasome contributes to the mitigation of AD 64–66 . In the present study, the expression of Nrf2 was increased, and that of NLRP3 inflammasome‐related proteins was decreased in dorsal skin tissues from DNCB‐induced mice, indicating the activation of Nrf2 signalling and inactivation of NLRP3 inflammasome in AD mice, coinciding with previous results 64 .…”

Section: Discussionsupporting

confidence: 90%

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Esculentoside A ameliorates DNCB‐induced atopic dermatitis by suppressing the ROS‐NLRP3 axis via activating the Nrf2 pathway

Liu

Liao

2023

Clin Exp Pharma Physio

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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.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 90%

Esculentoside A ameliorates DNCB‐induced atopic dermatitis by suppressing the ROS‐NLRP3 axis via activating the Nrf2 pathway

Liu

Liao

2023

Clin Exp Pharma Physio

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“…The findings of the present study are consistent with those of previous studies in which glabridin, a major hydrophobic constituent found in the roots and rhizomes of Glycyrrhiza glabra L, effectively downregulated mast cell infiltration and decreased epidermal and dermal thickness [ 1 ]. Moreover, similar results were reported with the treatment of DNCB-induced mice with Angelica Yinzi, a classic ancient prescription [ 16 ]. Lee et al also reported decreased mast cell infiltration and epidermal and dermal thickness following treatment of DNCB-treated mice with Centella asiatica extract [ 27 ].…”

Section: Discussionsupporting

confidence: 80%

“…The findings of the present study followed the pattern of a previous study in which Peucedanum japonicum Thunberg, an herbal medicine, suppressed the phosphorylation of ERK [ 22 ]. Moreover, a study by Liu et al also reported similar results; Angelica Yinzi, a classic ancient prescription, blocks ERK, JNK, p38 phosphorylation [ 16 ]. MAPK activation has been identified as one of the major causes of AD because MAPK phosphorylation promotes inflammatory cell generation.…”

Section: Discussionmentioning

confidence: 75%

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Tenebrio molitor Larva Trypsin Hydrolysate Ameliorates Atopic Dermatitis in C57BL/6 Mice by Targeting the TLR-Mediated MyD88-Dependent MAPK Signaling Pathway

et al. 2022

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Atopic dermatitis (AD) is a widely researched chronic inflammatory skin disease with a complex etiology. The increased prevalence of AD necessitates exploration of natural sources as potential therapeutic agents with limited side effects. In the current study, a 1-chloro-2,4-dinitrobenzene (DNCB)-induced AD mouse model was used to examine the anti-AD effects of Tenebrio molitor trypsin hydrolysate (TMTH) and its underlying molecular mechanism. DNCB-treated mice were treated with TMTH (1 and 10 mg/kg), and prednisolone (3 mg/kg) was used as the positive control. Serum and skin tissue samples were collected for subsequent analyses. The expression levels of proteins linked to the myeloid differentiation primary response 88 (MyD88)-dependent mitogen-activated protein kinase (MAPK) signaling pathway and serum IgE levels were estimated via Western blotting technique and ELISA (enzyme-linked immunosorbent assay), respectively. Inflammatory cell infiltration and thickening of the dorsal skin were measured using toluidine blue and hematoxylin and eosin staining, respectively. Oral administration of TMTH significantly reduced mast cell infiltration and dermal and epidermal thickness. Moreover, TMTH treatment reduced serum IgE levels. Western blotting confirmed that TMTH treatment suppressed the MyD88-dependent MAPK signaling pathway. Therefore, TMTH substantially inhibited AD-like skin lesion formation via immunomodulation, showing considerable potential for AD treatment.

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Exogenous drug-induced mouse models of atopic dermatitis

Zheng,

Ren,

Liu

et al. 2024

Cytokine & Growth Factor Reviews

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Angelica Yinzi alleviates 1-chloro-2,4-dinitrobenzene-induced atopic dermatitis by inhibiting activation of NLRP3 inflammasome and down-regulating the MAPKs/NF-kB signaling pathway

Cited by 11 publications

References 44 publications

Esculentoside A ameliorates DNCB‐induced atopic dermatitis by suppressing the ROS‐NLRP3 axis via activating the Nrf2 pathway

Esculentoside A ameliorates DNCB‐induced atopic dermatitis by suppressing the ROS‐NLRP3 axis via activating the Nrf2 pathway

Tenebrio molitor Larva Trypsin Hydrolysate Ameliorates Atopic Dermatitis in C57BL/6 Mice by Targeting the TLR-Mediated MyD88-Dependent MAPK Signaling Pathway

Exogenous drug-induced mouse models of atopic dermatitis

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