Effect of NGR1 on the atopic dermatitis model and its mechanisms

Atopic dermatitis (AD) is a highly pruritic chronic inflammatory skin disease. Notoginsenoside R1 (NGR1), a unique ingredient of P. notoginseng which is a well-known medicinal herb for its long history of use in traditional Chinese medicine, has been identified to have various biologically active pr...

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Main Authors: Wang Mingmei, Ma Jianli
Format: Article
Language:English
Published: De Gruyter 2019-11-01
Series:Open Medicine
Subjects:
Online Access:https://doi.org/10.1515/med-2019-0099
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author Wang Mingmei
Ma Jianli
author_facet Wang Mingmei
Ma Jianli
author_sort Wang Mingmei
collection DOAJ
description Atopic dermatitis (AD) is a highly pruritic chronic inflammatory skin disease. Notoginsenoside R1 (NGR1), a unique ingredient of P. notoginseng which is a well-known medicinal herb for its long history of use in traditional Chinese medicine, has been identified to have various biologically active properties that include anti-inflammatory effects. However, the effects of NGR1 on AD remain unclear. Therefore, this study aimed to investigate the effect and mechanism of NGR1 on the in vitro cell model of AD induced by LPS stimulation. RAW264.7 cells were stimulated with 1 μg/ml LPS to establish the in vitro cell inflammation model of AD. RAW264.7 cells were treated with various concentrations of NGR1 (0.1, 1, and 10 μM); then, an MTT assay was performed to determine the cell viability. An ELISA assay detected the levels of pro-inflammatory cytokines (interleukin-1β, IL-1β; interleukin-6, IL-6; tumor necrosis factor-α, TNF-α). Additionally, NO production was measured using a nitrate/nitrite assay kit. Results indicated that LPS induced increases in the levels of TNFα, IL-1β, IL-6, and NO production was significantly reduced by NGR1 treatment in a dose-dependent manner. Further, NGR1 treatment inhibited the activation of the NF-κB pathway, and the NLRP3 inflammasome in LPS stimulated RAW264.7 macrophages. The study data indicated that NGR1 might relieve atopic dermatitis via inhibiting inflammation through suppressing the NF-κB signaling pathway and NLRP3 inflammasome activation.
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spelling doaj.art-3c70d2d49ce6439cb73566966369a6332022-12-22T03:28:07ZengDe GruyterOpen Medicine2391-54632019-11-0114184785310.1515/med-2019-0099med-2019-0099Effect of NGR1 on the atopic dermatitis model and its mechanismsWang Mingmei0Ma Jianli1Department of Pharmacy, Fourth Medical Center of PLA General Hospita, 51#Fucheng Road, Beijing 100037, ChinaDepartment of Pharmacy, Fourth Medical Center of PLA General Hospita, 51#Fucheng Road, Beijing 100037, ChinaAtopic dermatitis (AD) is a highly pruritic chronic inflammatory skin disease. Notoginsenoside R1 (NGR1), a unique ingredient of P. notoginseng which is a well-known medicinal herb for its long history of use in traditional Chinese medicine, has been identified to have various biologically active properties that include anti-inflammatory effects. However, the effects of NGR1 on AD remain unclear. Therefore, this study aimed to investigate the effect and mechanism of NGR1 on the in vitro cell model of AD induced by LPS stimulation. RAW264.7 cells were stimulated with 1 μg/ml LPS to establish the in vitro cell inflammation model of AD. RAW264.7 cells were treated with various concentrations of NGR1 (0.1, 1, and 10 μM); then, an MTT assay was performed to determine the cell viability. An ELISA assay detected the levels of pro-inflammatory cytokines (interleukin-1β, IL-1β; interleukin-6, IL-6; tumor necrosis factor-α, TNF-α). Additionally, NO production was measured using a nitrate/nitrite assay kit. Results indicated that LPS induced increases in the levels of TNFα, IL-1β, IL-6, and NO production was significantly reduced by NGR1 treatment in a dose-dependent manner. Further, NGR1 treatment inhibited the activation of the NF-κB pathway, and the NLRP3 inflammasome in LPS stimulated RAW264.7 macrophages. The study data indicated that NGR1 might relieve atopic dermatitis via inhibiting inflammation through suppressing the NF-κB signaling pathway and NLRP3 inflammasome activation.https://doi.org/10.1515/med-2019-0099atopic dermatitisnotoginsenoside r1inflammationnf-κb pathwaynlrp3 inflammasome
spellingShingle Wang Mingmei
Ma Jianli
Effect of NGR1 on the atopic dermatitis model and its mechanisms
Open Medicine
atopic dermatitis
notoginsenoside r1
inflammation
nf-κb pathway
nlrp3 inflammasome
title Effect of NGR1 on the atopic dermatitis model and its mechanisms
title_full Effect of NGR1 on the atopic dermatitis model and its mechanisms
title_fullStr Effect of NGR1 on the atopic dermatitis model and its mechanisms
title_full_unstemmed Effect of NGR1 on the atopic dermatitis model and its mechanisms
title_short Effect of NGR1 on the atopic dermatitis model and its mechanisms
title_sort effect of ngr1 on the atopic dermatitis model and its mechanisms
topic atopic dermatitis
notoginsenoside r1
inflammation
nf-κb pathway
nlrp3 inflammasome
url https://doi.org/10.1515/med-2019-0099
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