Anti-inflammatory and antioxidant properties of Schisandrin C promote mitochondrial biogenesis in human dental pulp cells

Int Endod J. 2018 Apr;51(4):438-447. doi: 10.1111/iej.12861. Epub 2017 Oct 7.

Abstract

Aim: To examine the properties of Schisandrin C as an anti-inflammatory and antioxidant compound, and whether its characteristics promote mitochondrial biogenesis in human dental pulp cells (HDPCs).

Methodology: HDPCs were extracted from fresh third molars and cultured for experiments. Reactive oxidative stress (ROS) and nitric oxide (NO) formation were analysed by a Muse cell analyser. Western blotting and gelatin zymography were used to identify the presence of antioxidants, as well as anti-inflammatory and mitochondrial biogenesis with specific antibody. An unpaired Student's t-test was used for statistical analysis.

Results: Schisandrin C inhibited lipopolysaccharide-stimulated inflammatory molecules; interleukin 1 beta, tumour necrosis factor alpha, intracellular adhesion molecule-1, vascular cell adhesion molecule-1, matrix metalloproteinase-2 and -9, NO production, ROS formation, nuclear factor kappa B translocation (P < 0.05) through the mitogen-activated protein kinase pathway. Schisandrin C increased the expression of superoxide dismutase enzymes as well as haem oxygenase-1 and peroxisome proliferator-activated receptor gamma coactivator 1-alpha through the phosphorylated-protein kinase B (p-Akt) and nuclear factor erythroid 2-related factor-2 pathways (P < 0.05). The anti-inflammatory and antioxidant properties of Schisandrin C promoted mitochondrial biogenesis.

Conclusions: Schisandrin C has the potential to reduce inflammation and oxidation and to promote mitochondrial biogenesis. Therefore, Schisandrin C may be considered for use as an anti-inflammatory compound for oral inflammation through mitochondrial biogenesis.

Keywords: HO-1; MAPKs; PGC-1α; reactive oxidative stress.

MeSH terms

  • Anti-Inflammatory Agents / pharmacology*
  • Antioxidants / pharmacology*
  • Cyclooctanes / pharmacology
  • Dental Pulp / cytology*
  • Dental Pulp / drug effects*
  • Gelatin
  • Heme Oxygenase (Decyclizing) / metabolism
  • Humans
  • Inflammation / metabolism
  • Interleukin-1beta / metabolism
  • Lignans / pharmacology*
  • Lipopolysaccharides / adverse effects
  • Matrix Metalloproteinase 2 / metabolism
  • Matrix Metalloproteinase 9 / metabolism
  • Mitochondria / metabolism
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-E2-Related Factor 2 / metabolism
  • NF-kappa B / metabolism
  • Nitric Oxide / metabolism
  • Organelle Biogenesis*
  • Oxidative Stress / drug effects
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / metabolism
  • Polycyclic Compounds / pharmacology*
  • Reactive Oxygen Species / metabolism
  • Signal Transduction / drug effects
  • Superoxide Dismutase / metabolism
  • Transcription Factors / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Antioxidants
  • Cyclooctanes
  • Interleukin-1beta
  • Lignans
  • Lipopolysaccharides
  • NF-E2-Related Factor 2
  • NF-kappa B
  • PPARGC1A protein, human
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Polycyclic Compounds
  • Reactive Oxygen Species
  • Transcription Factors
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Gelatin
  • schizandrin C
  • Heme Oxygenase (Decyclizing)
  • Superoxide Dismutase
  • Mitogen-Activated Protein Kinases
  • Matrix Metalloproteinase 2
  • Matrix Metalloproteinase 9