Regulatory effects and molecular mechanism of Trigonostemon reidioides on lipopolysaccharide‑induced inflammatory responses in RAW264.7 cells
- Ju Young Shin
- Jae‑Shin Kang
- Hye‑Woo Byun
- Eun‑Kyung Ahn
Affiliations: Bio‑Center, Gyeonggi Institute of Science and Technology Promotion, Suwon, Gyeonggi 443‑270, Republic of Korea, Biological Genetic Resources Utilization Division, National Institute of Biological Resources, Incheon 404‑708, Republic of Korea
- Published online on: August 21, 2017 https://doi.org/10.3892/mmr.2017.7297
Copyright: © Shin
et al. This is an open access article distributed under the
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Trigonostemon reidioides (Kurz) Craib has been traditionally used for the treatment of vomiting and asthma in Cambodia. However, the underlying molecular mechanisms of the anti‑inflammatory effect of T. reidioides extract remains unknown. The present study investigated the anti‑inflammatory activity and molecular action of an ethanol extract of T. reidioides (ETR) in lipopolysaccharide (LPS)‑induced RAW264.7 macrophage cells. Nitric oxide assays, ELISA, reverse transcription‑quantitative polymerase chain reaction and western blot analysis were used. ETR treatment inhibited the production of nitric oxide by downregulating inducible nitric oxide synthase expression, while exhibiting no significant cytotoxicity compared with macrophages treated with LPS‑alone. Consequently, ETR decreased the production of certain proinflammatory cytokines, including interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α. Additionally, ETR inhibited the activation of mitogen‑activated protein kinases (MAPKs), including extracellular signal‑regulated kinase, c‑Jun N‑terminal kinase and p38 MAPK, as well as the phosphatidylinositol 3‑kinase (PI3K)/Akt signaling pathway. These effects were mediated by inhibition of the nuclear localization of nuclear factor κ‑B (NF‑κB). Taken together, the results of the present study demonstrate that ETR may exert an anti‑inflammatory effect by inhibiting the expression of inflammatory mediators and cytokines via downregulation of the NF‑κB, PI3K/Akt and the MAPK signaling pathways in LPS‑stimulated macrophages. Based on these results, we hypothesize that ETR may be a potential therapeutic agent for the treatment of inflammatory disorders.