Volume 20 Issue 12
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Article Navigation >  Chinese Journal of General Practice  > 2022  >  20(12): 2002-2005
GAO Juan, WU Yan, ZHENG Zhi-jun, WANG Qing-yun, LIU Shu, DANG Ni. Effect of baicalin on expression of inflammatory factors in human gingival fibroblasts induced by lipopolysaccharide[J]. Chinese Journal of General Practice, 2022, 20(12): 2002-2005. doi: 10.16766/j.cnki.issn.1674-4152.002755
Citation: GAO Juan, WU Yan, ZHENG Zhi-jun, WANG Qing-yun, LIU Shu, DANG Ni. Effect of baicalin on expression of inflammatory factors in human gingival fibroblasts induced by lipopolysaccharide[J]. Chinese Journal of General Practice, 2022, 20(12): 2002-2005. doi: 10.16766/j.cnki.issn.1674-4152.002755
shu

Effect of baicalin on expression of inflammatory factors in human gingival fibroblasts induced by lipopolysaccharide

doi: 10.16766/j.cnki.issn.1674-4152.002755
  • 1.

    Department of Orthodontics, Guiyang Stomatological Hospital, Guiyang, Guizhou 550002, China

Funds:

 gzwjkj2020-1-162

  • Received Date: 2021-10-15
    Available Online: 2023-02-07
    Abstract
  •   Objective  To investigate the effects of baicalin on the injury of human gingival fibroblasts (HGFs) induced by Lipopolysaccharide (LPS) through PI3K/Akt/NF-κB signaling pathway and its mechanism.  Methods  LPS induced HGFs injury models were established and divided into normal control group, model group and model + baicalin (1, 10 and 20 μg/mL) groups. Each group was set with 3 repetitions. After treatment with different concentrations of baicalin, Western blotting was used to detect the expression of p-Akt, Akt and NF-κB p65, and the expressions of inflammatory factors TNF-α, IL-1β and IL-6 were detected by qPCR. After treated with PI3K inhibitor LY294002 for half an hour, baicalin was used to intervene, and the genes and proteins expressions of Akt, p-Akt, NF-κB p65, TNF-α, IL-1β and IL-6 were detected by qPCR and Western blotting.  Results  Compared with the model group, low, medium and high dose baicalin could effectively reduce the mRNA expression levels of TNF-α, IL-6 and IL-1β, promote the protein expression of P-Akt and inhibit the nuclear protein expression of NF-κB p65 in a dose-dependent manner (all P < 0.05). Compared with the model group, the expression of p-Akt in the model + baicalin group was increased (P < 0.05), and the expression of NF-κB p65 was decreased (P < 0.01). After the treatment of PI3K inhibitor LY294002, the expression level of p-Akt /Akt in the model + baicalin group was increased (0.63±0.18) compared with that in the model group (0.56±0.14, P < 0.05), and the expressions of NF-κB p65, IL-6, IL-1β and TNF-α in the model + baicalin group were decreased compared with those in the model group (all P < 0.01). After baicalin treated LY294002, the expression levels of p-Akt/Akt, NF-κB p65, IL-6, IL-1β and TNF-α were not significantly different from those of the model group.  Conclusion  Baicalin can inhibit the inflammatory response induced by LPS-induced human gingival fibroblast injury, and its mechanism may be related to promote the phosphorylation of Akt, inhibit NF-κB p65 nuclear transcription and the release of inflammatory factors.

     

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