Oral administration of paeoniflorin attenuates allergic contact dermatitis by inhibiting dendritic cell migration and Th1 and Th17 differentiation in a mouse model

Shi, Dongmei; Li, Xuefeng; Li, Dongmei; Zhao, Quanjing; Shen, Ya; Yan, Hongxia; Fu, Hongjun; Zheng, Hailin; Lu, Guangming; Qiu, Ying; Liu, Weida

doi:10.1016/j.intimp.2015.02.031

Cited by 34 publications

(13 citation statements)

References 40 publications

(56 reference statements)

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“…As opposed to AD and chronic urticaria, ACD involves a Type IV cell mediated hypersensitivity (also known as delayed type hypersensitivity) with Th1 lymphocytes [68]. Small molecular weight haptens or haptens conjugated to proteins induce keratinocytes to release pro-inflammatory cytokines [69].…”

Section: Allergic Contact Dermatitismentioning

confidence: 99%

Vitamin D in atopic dermatitis, chronic urticaria and allergic contact dermatitis

Quirk

Rainwater

Shure

et al. 2016

Expert Review of Clinical Immunology

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Summary Vitamin D influences allergen-induced pathways in the innate and adaptive immune system, and its potential immunomodulatory role in allergic skin disorders has been explored. This comprehensive review article provides an overview of the role of vitamin D in three common dermatologic conditions: atopic dermatitis (AD), chronic urticaria, and allergic contact dermatitis (ACD). Whereas the literature regarding vitamin D and AD has resulted in mixed findings, several studies have described an inverse relationship between vitamin D levels and AD severity, and improvement in AD with vitamin D supplementation. Similarly, several studies report an inverse relationship between vitamin D levels and severity of chronic urticaria. Although current research in humans remains limited, an increased likelihood of ACD has been demonstrated in vitamin D-deficient mice. Additional well-designed clinical trials will be necessary to determine whether vitamin D supplementation should be recommended for prevention or adjuvant treatment of these common dermatologic conditions.

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Section: Allergic Contact Dermatitismentioning

confidence: 99%

Vitamin D in atopic dermatitis, chronic urticaria and allergic contact dermatitis

Quirk

Rainwater

Shure

et al. 2016

Expert Review of Clinical Immunology

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“…Sung et al [ 9 ] used TMA intervention to modify an ACD mouse model and discussed the pharmacological effects of Achyranthis radix extract, which was proved to be an effective agent for treatment of ACD disease, the anti-inflammatory mechanism was that Achyranthis could attenuate the II-1 β and TNF- α level in the ACD mouse body. Similarly, oral administration of paeoniflorin was demonstrated to attenuate ACD by inhibiting dendritic cell migration and Th1 and Th17 differentiation in a mouse model [ 10 ]. Sun et al [ 11 ] found that the Eriobotrya japonica seed extract could increase the IL-10 and reduce the IFN- γ in the ACD rat.…”

Section: Introductionmentioning

confidence: 99%

The Anti-Inflammatory Effect of Fructus Kochiae on Allergic Contact Dermatitis Rats via pERK1/2/TLR4/NF-κB Pathway Activation

Xiao

Yongning

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Allergic contact dermatitis (ACD) is a common irritability skin disease, which can be cured by using the Chinese patent medicine. To explore the pharmacological effect of total flavonoids of Fructus Kochiae (FK) on ACD, we used dinitrochlorobenzene- (DNCB-) induced ACD rats. Five groups were used in our experiments. The normal group and the DNCB group were treated with 0.5% CMC-Na; the DNCB + hFK group was treated with a high dose of total flavonoids of FK (200 mg/kg); the DNCB + lFK group was treated with a low dose of FK (100 mg/kg); the DNCB + Pre group was treated with prednisolone acetate (2.5 mg/kg). The results showed that FK treatment had significantly attenuated the inflammation induced by DNCB. The increased concentration of cytokines including IL-6, IL-18, and IFN-γ in ACD rats could be reversed by the FK administration, while IL-10 expressed the opposite result; the expression level of TLR4, pERK1/2, and NF-κB could be downregulated by the treatment with FK in the ACD rat. In a word, the total flavonoids of the FK had an anti-inflammatory effect on the DNCB-induced ACD rat; this regulatory mechanism was highly possible based on the pERK1/2/TLR4-NF-κB pathway activation.

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“…For example, studies have demonstrated that PF could inhibit Th17 differentiation and attenuate skin inflammation of psoriasis [23]. In our previous studies, we also found that PF inhibits Th17 differentiation in response to DC-mediated ACD when being challenged with 1-chloro-2,4-dinitrobenze (DNCB) [22,24]. However, it is still not clear how PF regulates the maturation of DCs, the cytokines secretion, and differentiation of Th17 cells.…”

Section: Introductionmentioning

confidence: 97%

Paeoniflorin suppresses IL-6/Stat3 pathway via upregulation of Socs3 in dendritic cells in response to 1-chloro-2,4-dinitrobenze

Shi

Wang

Zheng

et al. 2016

International Immunopharmacology

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Oral administration of paeoniflorin attenuates allergic contact dermatitis by inhibiting dendritic cell migration and Th1 and Th17 differentiation in a mouse model

Cited by 34 publications

References 40 publications

Vitamin D in atopic dermatitis, chronic urticaria and allergic contact dermatitis

Vitamin D in atopic dermatitis, chronic urticaria and allergic contact dermatitis

The Anti-Inflammatory Effect of Fructus Kochiae on Allergic Contact Dermatitis Rats via pERK1/2/TLR4/NF-κB Pathway Activation

Paeoniflorin suppresses IL-6/Stat3 pathway via upregulation of Socs3 in dendritic cells in response to 1-chloro-2,4-dinitrobenze

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