Immunosuppressive effect of hispidulin in allergic contact dermatitis

Thitilertdecha, Premrutai; Pluangnooch, Panwadee; Timalsena, Sunita; Soontrapa, Kitipong

doi:10.1186/s12906-019-2689-z

Cited by 11 publications

(5 citation statements)

References 16 publications

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“…To evaluate the action of DYRK1B inhibitor toward ACD, the murine CHS model was sensitized with 2,4-dinitrofluorobenzene (DNFB) 17 – 20 (Fig. 1 A).…”

Section: Resultsmentioning

confidence: 99%

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Inhibition of DYRK1B suppresses inflammation in allergic contact dermatitis model and Th1/Th17 immune response

Wongchang

Pluangnooch

Hongeng

et al. 2023

Sci Rep

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Allergic contact dermatitis (ACD) is a type IV hypersensitivity mainly mediated by Th1/Th17 immune response. Topical corticosteroid is currently the first-line treatment for allergic contact dermatitis (ACD) and systemic administration of immunosuppressive drugs are used in patients with severe disseminated cases. However, increased risk of adverse effects has limited their use. Thus, the development of a novel immunosuppressant for ACD with low toxicity is a challenging issue. In this study, we began our study by using a murine contact hypersensitivity (CHS) model of ACD to examine the immunosuppressive effects of DYRK1B inhibition. We found that mice treated with a selective DYRK1B inhibitor show reduced ear inflammation. In addition, a significant reduction of Th1 and Th17 cells in the regional lymph node upon DYRK1B inhibition was observed by FACS analysis. Studies in vitro further revealed that DYRK1B inhibitor does not only suppressed Th1 and Th17 differentiation, but also promotes regulatory T cells (Treg) differentiation. Mechanistically, FOXO1 signaling was enhanced due to the suppression of FOXO1Ser329 phosphorylation in the presence of DYRK1B inhibitor. Therefore, these findings suggest that DYRK1B regulates CD4 T cell differentiation through FOXO1 phosphorylation and DYRK1B inhibitor has a potential as a novel agent for treatment of ACD.

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“…To evaluate the action of DYRK1B inhibitor toward ACD, the murine CHS model was sensitized with 2,4-dinitrofluorobenzene (DNFB) 17 – 20 (Fig. 1 A).…”

Section: Resultsmentioning

confidence: 99%

“…DNFB was used as a hapten for inducing murine CHS as described by Honda et al and Thitilertdecha et al 19 , 20 . All mice were sensitized by painting 25 μL of 0.5% DNFB diluted in acetone and olive oil (4:1, v/v) on the shaved abdomen (day 0) with an average coverage area of 2 cm 2 .…”

Section: Methodsmentioning

confidence: 99%

Inhibition of DYRK1B suppresses inflammation in allergic contact dermatitis model and Th1/Th17 immune response

Wongchang

Pluangnooch

Hongeng

et al. 2023

Sci Rep

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“…AD is clinically characterized by its itchy, inflamed skin, and susceptibility to skin infections caused by skin barrier abnormalities [9][10][11]. AD is caused by various factors such as genetic factors, and is triggered by environmental pollutants, stress, resulting in cell mediated immune responses which may cause dysfunction with the skin's function as a barrier [12]. Several studies have suggested that AD is related with a Th1/Th2 imbalance, but recently Th17 and Th22 cells have been reported to also play a significant role in the disease.…”

Section: Discussionmentioning

confidence: 99%

“…In all the stages of AD, Th2 cells play a dominant role as the increase of the Type 2 cytokines and chemokines such as IL-4, IL-5, IL-10, IL-13, IL-31 are evident. These mediators are involved in allergic responses impairing keratinocyte differentiation [12]. In particular, Th17 cells which are defined by production of IL-17 and IL-22, show an increase in number but decrease in activity [12,13].…”

Section: Discussionmentioning

confidence: 99%

Effect of Bee Venom Pharmacopuncture on Inflammation in Mouse Model of Induced Atopic Dermatitis

Park

Song

2020

J Acupunct Res

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Background: This study was designed using a mouse model of atopic dermatitis [phthalic anhydride (PA)-treated mice], to investigate the anti-inflammatory effect of bee venom pharmacopuncture (BVP) in keratinocytes.Methods: Western blot analysis was performed to investigate inflammation related protein expression of iNOS, COX-2, phospho-ERK (p-ERK), and ERK, in LPS (1 μg/mL)-activated keratinocytes, following BVP treatment, and in PA-treated mice, after BVP treatment. Griess reaction was performed to investigate NO concentration. Enzyme-linked immunosorbent assays were used to determine the concentrations of interleukin (IL)-4+, IL-17A+, IL-13 and IL-4 in PA-treated mice after BVP treatment. In addition, monocyte, macrophage, neutrophil, and eosinophil counts were measured to observe the changes in white blood cell infiltration.Results: The keratinocytes of the BVP-treated group showed a decreased expression of iNOS, COX-2, ERK at 5 OX-2, ERK E, and p-ERK at 1, 2 and 5 RKRK ERK ERK, and a dose-dependent decrease in NO concentration at 2 and 5 ntrationof s. In the BVP-treated groups (0.1 μ.1-trea μ.1-treated gr), PA-treated mice showed recovery after 4 weeks which was dose-dependent, showing a significant decrease in clinical scores for AD, and a decreased concentration of IL-13 and IL-4 with BV treatment. There was a dose-dependent decrease in the infiltration of eosinophils, neutrophils, monocytes, macrophages, and a decreased thickness of the epidermis due to inflammation, and decreased expressions of iNOS, COX-2, p-ERK, ERK, especially in the 0.1 μ0/mL BVP-treated group,<br>Conclusion: These results suggest that BVP may be an effective alternative treatment for atopic dermatitis.

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“…Luteolin has also been found to exhibit protective activities against LPSinduced AKI in mice model (Xin et al, 2016). As a natural flavonoid, hispidulin has been identified as the active ingredient in a few traditional Chinese medicines such as Artemisia vestita and Arnica montana L. Hispidulin has displayed a variety of pharmacological properties, including anticancer, anti-fungal, anti-diabetic, immunosuppressive, and neuroprotective activities (Thitilertdecha et al, 2019). Moreover, a recent report has documented that hispidulin suppressed mast cell-mediated allergic inflammation in vitro and in vivo (Kim et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

HSA-MIR-203/MyD88 axis mediates the protective effect of hispidulin on LPS-induced apoptosis in a human renal tubular epithelial line, HK-2

WANG¹,

LIU²,

Han³

et al. 2022

Biocell

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Acute kidney injury (AKI), commonly occurring as complications of sepsis, cardiac surgery, and liver or kidney transplantation, is a critical care syndrome. It is well known that lipopolysaccharide (LPS) shock is a common triggering factor for AKI. This study is aimed to examine the effect of flavonoid compound hispidulin on LPS-induced AKI. For this, renal tubular epithelial cell HK-2 was treated with LPS to establish an in vitro model of AKI. The effect of hispidulin on HK-2 cell viability was examined using CCK-8 assay. Cell apoptosis was determined by TUNEL and flow cytometry. Apoptosis marker proteins were determined by using western blot. The levels of pro-inflammatory cytokines were determined by ELISA assay and qRT-PCR. The translocation of NF-κB was determined by western blot. The effect of MyD88 on the cytoprotective activities of hispidulin was examined by overexpressing MyD88 in HK-2 cells. Our results showed that hispidulin was not able to produce a cytotoxic effect on HK-2 cells at tested concentrations.However, hispidulin could protect HK-2 cells from LPS-induced cell injury. Our results also showed that hispidulin was able to attenuate LPS-induced HK-2 cell apoptosis. In addition, LPS led to an inflammatory response in HK-2 cells, evidenced by NF-κB p65 activation as well as increased expression and release of inflammatory cytokine IL-6 and TNFα, which could be reversed by pretreatment with hispidulin. Overexpression MyD88 was found to significantly dampen the cytoprotective activities of hispidulin against LPS insult. More importantly, MyD88 was identified as a direct target of hsa-miR-203, and hispidulin was found to regulate the expression of MyD88 via upregulating hsa-miR-203. Our results showed that hispidulin attenuates LPS-induced HK-2 damage via regulating hsa-miR-203/MyD88 axis.

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Immunosuppressive effect of hispidulin in allergic contact dermatitis

Cited by 11 publications

References 16 publications

Inhibition of DYRK1B suppresses inflammation in allergic contact dermatitis model and Th1/Th17 immune response

Inhibition of DYRK1B suppresses inflammation in allergic contact dermatitis model and Th1/Th17 immune response

Effect of Bee Venom Pharmacopuncture on Inflammation in Mouse Model of Induced Atopic Dermatitis

HSA-MIR-203/MyD88 axis mediates the protective effect of hispidulin on LPS-induced apoptosis in a human renal tubular epithelial line, HK-2

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