Article Publish Status: FREE
Abstract Title:

Tocotrienol regulates osteoclastogenesis in rheumatoid arthritis.

Abstract Source:

Korean J Intern Med. 2021 03 ;36(Suppl 1):S273-S282. Epub 2020 Jun 19. PMID: 32550719

Abstract Author(s):

Kyoung-Woon Kim, Bo-Mi Kim, Ji-Yeon Won, Hong Ki Min, Seoung Joon Lee, Sang-Heon Lee, Hae-Rim Kim

Article Affiliation:

Kyoung-Woon Kim


BACKGROUND/AIMS: The present study aimed to investigate whether tocotrienol regulates interleukin 17 (IL-17)-induced osteoclastogenesis in rheumatoid arthritis (RA).

METHODS: We evaluated the effect of tocotrienol on IL-17-induced receptor activator of nuclear factor kappa B ligand (RANKL) production using RA fibroblast-like synoviocyte (FLS), together with real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Osteoclast differentiation was confirmed after culturing IL-17-treated RA FLS and Th17 cells with tocotrienol and monocytes. We analyzed the suppressive effect of tocotrienol on Th17 cells percentage or Th17-cytokine levels among peripheral blood mononuclear cells using flow cytometry.

RESULTS: We found that IL-17 stimulated FLS to produce RANKL and tocotrienol decreased this IL-17-induced RANKL production. Tocotrienol decreased the IL-17-induced activation of mammalian target of rapamycin, extracellular signal-regulated kinase, and inhibitor of kappa B-alpha. When monocytes were incubated with IL-17, RANKL, IL-17-treated FLS or Th17 cells, osteoclasts were differentiated and tocotrienol decreased this osteoclast differentiation. Tocotrienol reduced Th17 cell differentiation and the production of IL-17 and sRANKL; however, tocotrienol did not affect Treg cell differentiation.

CONCLUSION: Tocotrienol inhibited IL-17- activated RANKL production in RA FLS and IL-17-activated osteoclast formation. In addition, tocotrienol reduced Th17 differentiation. Therefore, tocotrienol could be a new therapeutic choice to treat bone destructive processes in RA.

Study Type : In Vitro Study

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