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Abstract
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.
Highlights
Atopic dermatitis (AD) is a highly pruritic chronic inflammatory skin disease
The levels of tumor necrosis factor-α (TNF-α), IL-1β, and IL-6 in the culture supernatants of RAW264.7 macrophages were detected by ELISA
The present study demonstrated that Notoginsenoside R1 (NGR1) significantly reduced the levels of pro-inflammatory cytokines and NO production that were enhanced by LPS stimulation in
Summary
Abstract: Atopic dermatitis (AD) is a highly pruritic chronic inflammatory skin disease. 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); an MTT assay was performed to determine the cell viability. 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. 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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