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Anti-inflammatory effect of quercetin and galangin in LPS-stimulated RAW264.7 macrophages and DNCB-induced atopic dermatitis animal models

Cited 137 time in Web of Science Cited 157 time in Scopus
Authors

Le, Hae Nim; Shin, Seong Ah; Choo, Gang Sik; Kim, Hyeong Jin; Park, Young Seok; Kim, Byeong Soo; Kim, Sang Ki; Cho, Sung Dae; Nam, Jeong Seok; Choi, Chang Sun; Che, Jeong Hwan; Park, Byung Kwon; Jung, Ji Youn

Issue Date
2018-02
Publisher
Demetrios A. Spandidos Ed. & Pub.
Citation
International Journal of Molecular Medicine, Vol.41 No.2, pp.888-898
Abstract
Flavonols are compounds that have been shown to possess potent anti-inflammatory effects in cellular and animal models of inflammation. In the present study, the anti-inflammatory effects and mechanisms of two natural flavonols, quercetin and galangin, in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages were investigated. It was identified that quercetin and galangin markedly reduced the production of nitric oxide (NO), inducible NO synthase and interleukin-6, and the nuclear translocation of nuclear factor-kappa B (NF-kappa B). In addition, LPS-induced activation of extracellular signal-regulated kinase 1/2 (Erk1/2) and c-Jun N-terminal kinase (JNK) was suppressed by quercetin and galangin. Taken together, these data implied that NF-kappa B, Erk1/2 and JNK may be potential molecular targets of quercetin and galangin in an LPS-induced inflammatory response. Subsequently, the effects of oral administration of quercetin or galangin, either alone or in combination, in a 2,4-dinitrochlorobenzene-induced atopic dermatitis (AD) mouse model were investigated. As a result, measurements of ear thickness and the levels of serum immunoglobulin E, and histological analysis revealed that the two flavonols led to a decrease in inflammation, whereas, in combination, they were even more effective. These results suggested that quercetin and galangin may be promising therapeutic agents for AD. Additionally, their combination may be a novel therapeutic strategy for the prevention of AD.
ISSN
1107-3756
Language
English
URI
https://hdl.handle.net/10371/149209
DOI
https://doi.org/10.3892/ijmm.2017.3296
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