Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside isolated from the flowers of Hosta plantaginea exerts anti-inflammatory activity via suppression of NF-?B, MAPKs and Akt pathways in RAW 264.7 cells

Kaempferol 3-O-(2(G)-glucosylrutinoside)-7-O-glucoside (KGG) has isolated from Hosta plantaginea flowers and possessed an inhibitory effect on cyclooxygenase 2 (COX-2), could be effective in inhibiting inflammation. However, the anti-inflammatory activity and mechanism of KGG remain unknown. In this study, for the first time, the anti-inflammatory effect of KGG and its potential molecular mechanisms were explored in cells. KGG had no cytotoxicity at concentrations of 1.25, 2.5, 5, 10, 20, and 40 mu M by Cell Counting kit-8 assay in RAW 264.7 cells. Besides, KGG concentration-dependently (1.25, 2.5, and 5 mu M) inhibited secretions of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), and IL-6 in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Western blot showed that the phosphorylation of nuclear factor kappa-B (NF-kappa B) p65, inhibitor of NF-kappa B (I kappa B), p38 MAPK, c-Jun N-terminal kinases (JNK), extracellular signal-regulated kinase (Erk), and protein kinase B (Akt), together with inducible nitric oxide synthase (iNOS) and COX-2 were significantly attenuated by KGG (1.25, 2.5, and 5 mu M) in a concentration-dependent relationship. Meanwhile, KGG remarkably enhanced the protein expression of I kappa B. Taken together, KGG may be one of bioactive phytochemicals from H. plantaginea flowers, and be an anti-inflammatory agent via inhibiting NF-kappa B, mitogen-activated protein kinases (MAPKs), and Akt signaling pathways.

Automated summary

This study explored the anti-inflammatory effect and potential molecular mechanisms of Kaempferol 3-O-(2(G)-glucosylrutinoside)-7-O-glucoside (KGG) in cells. KGG inhibited the secretion of inflammatory mediators and attenuated the activation of NF-kappa B, MAPKs, and Akt signaling pathways.