Journal of Dental Sciences (Jan 2022)

Effects of baicalin on the proliferation and expression of OPG and RANKL in human cementoblast-lineage cells

  • Ryo Kunimatsu,
  • Aya Kimura,
  • Shuzo Sakata,
  • Yuji Tsuka,
  • Yuki Yoshimi,
  • Takaharu Abe,
  • Isamu Kado,
  • Yuka Yashima,
  • Jin Izumino,
  • Ayaka Nakatani,
  • Masae Kitagawa,
  • Mutsumi Miyauchi,
  • Takashi Takata,
  • Kotaro Tanimoto

Journal volume & issue
Vol. 17, no. 1
pp. 162 – 169

Abstract

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Background/purpose: Baicalin, a natural bioactive flavonoid extracted from Scutellaria baicalensis Georgi, mediates bone metabolism, and recent studies have revealed that it has cell signaling properties. However, its biological functions in cementoblasts still remain unclear. This study therefore aimed to investigate the effects of baicalin on bone resorption markers, including osteoprotegerin (OPG) and receptor activator of nuclear factor-κβ ligand (RANKL), in human cementoblast-lineage cells, as well as their proliferation ability. Materials and methods: Human cementoblast cell line (HCEM) cells were cultured and treated with 0, 0.01, 0.1, or 1 μM of baicalin. The proliferative capacity of cultured HCEM cells was analyzed using bromodeoxyuridine immunoassay and cell counting. The baicalin effect on OPG and RANKL expression was determined using quantitative polymerase chain reaction (qPCR) and western blotting. Furthermore, OPG expression was measured in 1 μM baicalin-treated HCEM cells in the presence or absence of the Wnt signaling pathway inhibitor, Dickkopf (Dkk)-1, using qPCR and western blotting. Results: The addition of 0.01, 0.1, and 1 μM of baicalin did not significantly change the proliferative capacity of cultured HCEM cells. Compared with the non-supplemented group, baicalin increased and suppressed OPG and RANKL gene and protein expression, respectively, in a concentration-dependent manner. OPG mRNA and protein expression levels were increased by 1 μM baicalin, which was suppressed by Dkk-1 addition. Conclusion: Baicalin enhanced OPG expression in HCEM cells through the Wnt/beta-catenin signaling pathway, which could contribute to periodontal tissue regeneration.

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