Effects of Shock Waves on Expression of IL-6, IL-8, MCP-1, and TNF-α Expression by Human Periodontal Ligament Fibroblasts: An In Vitro Study

Med Sci Monit. 2016 Mar 20:22:914-21. doi: 10.12659/msm.897507.

Abstract

Background: Extracorporeal shock wave therapy (ESWT) can modulate cell behavior through mechanical information transduction. Human periodontal ligament fibroblasts (hPDLF) are sensible to mechanical stimulus and can express pro-inflammatory molecules in response. The aim of this study was to evaluate the impacts of shock waves on interleukin-6 (IL-6), interleukin-8 (IL-8), monocyte chemotactic protein 1 (MCP-1), and tumor necrosis factor-alpha (TNF-α) expression by hPDLF.

Material/methods: After being treated by shock waves with different parameters (100-500 times, 0.05-0.19 mJ/mm(2)), cell viability was tested using CCK-8. IL-6, IL-8, MCP-1, and TNF-α gene expression was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) and IL-6 and IL-8 protein was measured by enzyme-linked immunosorbent assay (ELISA) at different time points.

Results: Shock waves with the parameters used in this study had no significant effects on the viability of hPDLF. A statistical inhibition of IL-6, IL-8, MCP-1, and TNF-α expression during the first few hours was observed (P<0.05). Expression of IL-8 was significantly elevated in the group receiving the most pulses of shock wave (500 times) after 4 h (P<0.05). At 8 h and 24 h, all treated groups demonstrated significantly enhanced IL-6 expression (P<0.05). TNF-α expression in the groups receiving more shock pulses (300, 500 times) or the highest energy shock treatment (0.19 mJ/mm(2)) was statistically decreased (P<0.05) at 24 h.

Conclusions: Under the condition of this study, a shock wave with energy density no higher than 0.19 mJ/mm(2) and pulses no more than 500 times elicited no negative effects on cell viability of hPDLF. After a uniform initial inhibition impact on expression of inflammatory mediators, a shock wave could cause dose-related up-regulation of IL-6 and IL-8 and down-regulation of TNF-α.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Cell Proliferation
  • Cell Survival / genetics
  • Chemokine CCL2 / genetics*
  • Chemokine CCL2 / metabolism
  • Fibroblasts / cytology
  • Fibroblasts / metabolism*
  • Gene Expression Regulation*
  • High-Energy Shock Waves*
  • Humans
  • Interleukin-6 / genetics*
  • Interleukin-6 / metabolism
  • Interleukin-8 / genetics*
  • Interleukin-8 / metabolism
  • Male
  • Periodontal Ligament / cytology*
  • Time Factors
  • Tumor Necrosis Factor-alpha / genetics*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • CCL2 protein, human
  • CXCL8 protein, human
  • Chemokine CCL2
  • IL6 protein, human
  • Interleukin-6
  • Interleukin-8
  • Tumor Necrosis Factor-alpha