期刊
BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
卷 19, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12906-019-2720-4
关键词
Anti-inflammation; Anti-osteoclastogenesis; Inflammatory diseases; Vaccinium oldhamii
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [NRF-2016R1D1A3B03931713, NRF-2018R1A6A1A03024862]
Background Vaccinium oldhamii (V. oldhamii) has been reported to exert a variety of the pharmacological properties such as anti-oxidant activity, anti-cancer activity, and inhibitory activity of alpha-amylase and acetylcholinesterase. However, the anti-inflammatory activity of V. oldhamii has not been studied. In this study, we aimed to investigate anti-inflammatory activity of the stem extracts from V. oldhamii, and to elucidate the potential mechanisms in LPS-stimulated RAW264.7 cells. Methods Cell viability was evaluated by MTT assay. The determination of NO and PGE2 production was performed using Griess reagent and Prostaglandin E-2 ELISA Kit, respectively. The change of mRNA or protein level was evaluated by RT-PCR and Western blot. Results Among VOS, VOL and VOF, the inhibitory effect of NO and PGE(2) production induced by LPS was highest in VOS treatment. Thus, VOS was selected for the further study. VOS dose-dependently blocked LPS-induced NO and PGE(2) production by inhibiting iNOS and COX-2 expression, respectively. VOS inhibited the expression of pro-inflammatory cytokines such as IL-1 beta, IL-6 and TNF-alpha. In addition, VOS suppressed TRAP activity and attenuated the expression of the osteoclast-specific genes such as NFATc1, c-FOS, TRAP, MMP-9, cathepsin K, CA2, OSCAR and ATPv06d2. VOS inhibited LPS-induced NF-kappa B signaling activation through blocking I kappa B-alpha degradation and p65 nuclear accumulation. VOS inhibited MAPK signaling activation by attenuating the phosphorylation of ERK1/2, p38 and JNK. Furthermore, VOS inhibited ATF2 phosphorylation and blocked ATF2 nuclear accumulation. Conclusions These results indicate that VOS may exert anti-inflammatory activity by inhibiting NF-kappa B and MAPK/ATF2 signaling. From these findings, VOS has potential to be a candidate for the development of chemopreventive or therapeutic agents for the inflammatory diseases.
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