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

作者：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^*

来源：International Journal of Molecular Medicine, 2018, 41(2): 888-898.

DOI：10.3892/ijmm.2017.3296

• hydroxy group
• flavonol
• anti-inflammation
• nuclear factor-kappa B
• mitogen-activated protein kinase

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.

• 出版日期2018-2