Therapeutic effects of quinine in a mouse model of atopic dermatitis

Zhang, Qian; Jiang, Hongjing; Liu, Miao; Li, Xinchen; Zhou, Murong; Lyu, Yansi; Huang, Jingkai; Chen, Si; Wang, Li

doi:10.3892/mmr.2021.11952

Cited by 7 publications

(10 citation statements)

References 43 publications

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“…While Flg was downregulated in the moderate hlAD lesions at day 12, the expression was upregulated at the end of the experiment, indicating mild hlAD. This finding is in line with the results from the literature, where Flg downregulation is described for DNCB-induced moderate to severe hlAD [ 21 , 60 , 61 ] but not for mild hlAD [ 27 ] or mild human AD [ 62 ]. Krt10, an early differentiation marker, remained unchanged by DNCB treatment in our study.…”

Section: Discussionsupporting

confidence: 92%

Characterization of Different Inflammatory Skin Conditions in a Mouse Model of DNCB-Induced Atopic Dermatitis

Riedl,

Kühn,

Hupfer

et al. 2023

Inflammation

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The mouse model of 2,4-dinitrochlorbenzene (DNCB)-induced human-like atopic dermatitis (hlAD) has been widely used to test novel treatment strategies and compounds. However, the study designs and methods are highly diverse, presenting different hlAD disease patterns that occur after sensitization and repeated challenge with DNCB on dorsal skin. In addition, there is a lack of information about the progression of the disease during the experiment and the achieved pheno- and endotypes, especially at the timepoint when therapeutic treatment is initiated. We here examine hlAD in a DNCB-induced BALB/cJRj model at different timepoints: (i) before starting treatment with dexamethasone, representing a standard drug control (day 12) and (ii) at the end of the experiment (day 22). Both timepoints display typical AD-associated characteristics: skin thickening, spongiosis, hyper- and parakeratosis, altered cytokine and gene expression, increased lipid mediator formation, barrier protein and antimicrobial peptide abnormalities, as well as lymphoid organ hypertrophy. Increased mast cell infiltration into the skin and elevated immunoglobulin E plasma concentrations indicate a type I allergy response. The DNCB-treated skin showed an extrinsic moderate sub-acute hlAD lesion at day 12 and an extrinsic mild sub-acute to chronic pheno- and endotype at day 22 with a dominating Th2 response. A dependency of the filaggrin formation and expression in correlation to the disease severity in the DNCB-treated skin was found. In conclusion, our study reveals a detailed classification of a hlAD at two timepoints with different inflammatory skin conditions and pheno- and endotypes, thereby providing a better understanding of the DNCB-induced hlAD model in BALB/cJRj mice.

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Section: Discussionsupporting

confidence: 92%

Characterization of Different Inflammatory Skin Conditions in a Mouse Model of DNCB-Induced Atopic Dermatitis

Riedl,

Kühn,

Hupfer

et al. 2023

Inflammation

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“…For example, DNFB is an irritant at a concentration of 0.05%, but geraniol is an irritant at 50% (18). In the study of Zhang et al (2), a 100 µL mixture of 0.5% DNCB and acetone/olive oil (3: 1) was applied to the shaved area for one and two days. In another study, to create a mouse model of ICD, a 20 µL mixture of 0.5% DNCB with olive oil/acetone (4: 1) was applied to the left ear of mice (8).…”

Section: Discussionmentioning

confidence: 99%

“…Finally, we induced irritant contact dermatitis models after the 10th day of DNCB application. Nevertheless, in the study of Zhang et al (2), atopic dermatitis models were induced after 28 days of DNCB application. Furthermore, DNCB was used to induce atopic dermatitis at different dilutions and for longer periods (19,20).…”

Section: Discussionmentioning

confidence: 99%

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Mouse Model of Irritant Contact Dermatitis

et al. 2022

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Background: Irritant contact dermatitis is a common inflammatory skin disease characterized by skin barrier dysfunction, eczematous dermatitis, and chronic itching. This disease severely affects the quality of life. Considering that the current treatment approaches are not ideal, more extensive research is needed to develop new treatments. Mainly, a mouse model is needed to investigate the effectiveness of new drugs to treat this disease. Objectives: This study was conducted to create a mouse model of irritant contact dermatitis. Methods: In the current study, we used BALB/c female mice to prepare a mouse model of irritant contact dermatitis. To induce irritant contact dermatitis, we used a dinitrochlorobenzene mixture with acetone/olive oil as an irritant. After 10 days of application, the mouse skin tissue was isolated and examined in terms of histopathology. Results: The introduced protocol created an irritant contact dermatitis model clinically and histopathologically. Conclusions: In the present study, we introduced a new protocol using a mixture of dinitrochlorobenzene and acetone/olive oil to create an irritant contact dermatitis model. Mouse models have been extensively used to discover the complex mechanisms of irritant contact dermatitis and provide a preclinical platform before conducting clinical interventional research on humans to evaluate a new therapeutic approach. However, one should always look for models that cause the least pain and suffering in the animal and simultaneously are simple and reliable for the desired studies. Thus, our protocol is a new approach that can be effective and painless in creating a model of irritant contact dermatitis.

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“…For this reason, HIF-1α activation is largely responsible for poor treatment outcomes. HIF-1α is known to play an important role in hypoxia-induced angiogenesis, metastasis ( Xing et al, 2011 ; Bocca et al, 2014 ), EMT and invasion of cancer cells ( Jo et al, 2009 ; Xing et al, 2011 ; Bocca et al, 2014 ; Zhang et al, 2021 ; Zhang et al, 2022 ), and also in inducing conventional drug-resistant properties ( Yu et al, 2012 ), thus playing a central role in tumor cell malignancy. Moreover, as the success of targeted monotherapy is uncertain, scientists have aimed in identifying agents that could target and interfere with multiple subcellular cell signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Calebin A targets the HIF-1α/NF-κB pathway to suppress colorectal cancer cell migration

Brockmueller,

Girisa,

Motallebi

et al. 2023

Front. Pharmacol.

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Background: Hypoxia-inducible factor-1α (HIF-1α) is one of the major tumor-associated transcription factors modulating numerous tumor properties such as tumor cell metabolism, survival, proliferation, angiogenesis, and metastasis. Calebin A (CA), a compound derived from turmeric, is known for its anti-cancer activity through modulation of the NF-κB pathway. However, its impact on HIF-1α in colorectal cancer (CRC) cell migration is unknown.Methods: Human CRC cells (HCT-116) in 3D alginate and monolayer multicellular TME (fibroblasts/T lymphocytes) were subjected to CA or the HIF-1α inhibitor to explore the efficacy of CA on TME-induced inflammation, migration, and tumor malignancy.Results: CA significantly inhibited TME-promoted proliferation and migration of HCT-116 cells, similar to the HIF-1α inhibitor. Colony formation, toluidine blue staining, and immunolabeling showed that CA inhibited the migration of HCT-116 cells partly by inhibiting HIF-1α, which is critical for CRC cell viability, and these observations were confirmed by electron microscopy. In addition, Western blot analysis confirmed that CA inhibited TME-initiated expression of HIF-1α and biomarkers of metastatic factors (such as NF-κB, β1-integrin, and VEGF), and promoted apoptosis (caspase-3), in a manner comparable to the HIF-1α inhibitor. Finally, TME induced a purposeful pairing between HIF-1α and NF-κB, suggesting that the synergistic interplay between the two tumor-associated transcription factors is essential for CRC cell malignancy and migration and that CA silences these factors in tandem.Conclusion: These results shed light on a novel regulatory modulation of CA signaling in CRC cell migration, partially via HIF-1α/NF-κB with potentially relevant implications for cancer therapy.

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Therapeutic effects of quinine in a mouse model of atopic dermatitis

Cited by 7 publications

References 43 publications

Characterization of Different Inflammatory Skin Conditions in a Mouse Model of DNCB-Induced Atopic Dermatitis

Characterization of Different Inflammatory Skin Conditions in a Mouse Model of DNCB-Induced Atopic Dermatitis

Mouse Model of Irritant Contact Dermatitis

Calebin A targets the HIF-1α/NF-κB pathway to suppress colorectal cancer cell migration

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