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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Format: | Article |
Language: | English |
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De Gruyter
2019-11-01
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Series: | Open Medicine |
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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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format | Article |
id | doaj.art-3c70d2d49ce6439cb73566966369a633 |
institution | Directory Open Access Journal |
issn | 2391-5463 |
language | English |
last_indexed | 2024-04-12T14:59:54Z |
publishDate | 2019-11-01 |
publisher | De Gruyter |
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series | Open Medicine |
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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