Abstract
Aim
To examine the properties of Schisandrin C as an anti-inflammatory and anti-oxidant 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 analyzed by a Muse cell analyzer. Western blotting and gelatin zymography were used to identify the presence of anti-oxidants, 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 (LPS)-stimulated inflammatory molecules; interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), matrix metalloproteinase-2 and -9 (MMP-2/9), NO production, ROS formation, nuclear factor kappa B (NF-κB) translocation (P < 0.05) through the mitogen-activated protein kinase (MAPK) pathway. Schisandrin C increased the expression of superoxide dismutase (SOD) enzymes as well as heme oxygenase-1 (HO-1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) through the phosphorylated-protein kinase B (p-Akt) and nuclear factor erythroid 2-related factor-2 (Nrf-2) pathways (P < 0.05). The anti-inflammatory and anti-oxidant 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.
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