Comparative study on anti-inflammatory effect of Lonicerae Japonicae Flos and Lonicerae Flos / 中国中药杂志

ABSTRACT

The aim of this paper was to observe the anti-inflammatory action and mechanism of Lonicerae Japonicae Flos extract and Lonicerae Flos extract in xylene-induced ear swelling experiment and lipopolysaccharide(LPS)-induced RAW264.7 cell inflammatory model. In vivo, xylene-induced mouse auricle swelling model was used to detect the auricle swelling degree and swelling inhibition rate of Lonicerae Japonicae Flos extract and Lonicerae Flos extract; the pathological changes of mice auricle were observed by hematoxylin eosin(HE) staining. In vitro, RAW264.7 inflammatory cell model was induced by LPS, where the cytotoxic effects of Lonicerae Japonicae Flos extract and Lonicerae Flos extract on RAW264.7 cells were detected by CCK-8 method; Griess method was used to detect the effect of Lonicerae Japonicae Flos extract and Lonicerae Flos extract on nitric oxide(NO) production, and ELISA method was used to detect the content of inflammatory factors interleukin-6(IL-6), IL-1β, and tumor necrosis factor-α(TNF-α). At last, Western blot was used to detect the protein changes of cyclooxygenase 1(COX1), COX2 and inducible nitric oxide synthetase(iNOS) for RAW264.7 cells. The results showed that both Lonicerae Japonicae Flos extract and Lonicerae Flos extract could significantly inhibit the degree of auricle swelling caused by xylene in mice and the inhibition rate was positively correlated with the drug dose. Furthermore, both of them could reduce the infiltration of lymphocytes and neutrophils in mouse ear tissues. For in vitro experiments, both Lonicerae Japonicae Flos extract and Lonicerae Flos extract inhibited NO secretion in RAW264.7 cells, down-regulated the release of IL-1β, IL-6 and TNF-α, and down-regulated iNOS protein and COX2, NF-κB p65 protein content. In conclusion, both Lonicerae Japonicae Flos extract and Lonicerae Flos extract have good anti-inflammatory effect, and the mechanism may be related with the inhibition of NF-κB signaling pathway.