The effect of low-level laser irradiation on hyperglycemia-induced inflammation in human gingival fibroblasts.
Kun-Tsung Denzel LeeMin-Hsuan ChiangPing-Ho ChenMei-Ling HoHong-Zin LeeHuey-Er LeeYan-Hsiung WangPublished in: Lasers in medical science (2018)
Hyperglycemia-induced inflammation can greatly increase the risk of periodontal disease in people with diabetes. Low-level laser irradiation (LLLI) has been used for wound healing and anti-inflammation in many cases, and LLLI is known to inhibit the lipopolysaccharide (LPS)-stimulated inflammatory response. However, the therapeutic effect of LLLI in diabetes patients with periodontitis remains unknown. In this study, we cultured human gingival fibroblasts (HGFs) in high-glucose medium (35 mM) to mimic a hyperglycemic environment, and then measured the anti-inflammatory effect of LLLI by assessing the expression of pro-inflammatory genes including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and IL-8 by quantitative real-time polymerase chain reaction. The results demonstrated no significant inflammatory response in HGFs cultured in mannitol medium and in those treated only with LLLI. However, HGFs cultured only in high-glucose medium showed significantly higher expression of pro-inflammatory cytokine than in those treated together with LLLI. We then observed that LLLI reduced the expression of pro-inflammatory cytokines in HGFs cultured in high-glucose medium by modulating cAMP signaling. We also investigated whether antioxidant (vitamin C) treatment reduced the inflammatory effect of oxidative stress in HGFs cultured in high-glucose medium but found no additive effect upon co-treatment with LLLI, suggesting that LLLI may activate cAMP signaling, but not reactive oxygen species (ROS) signaling, to reduce the high glucose-induced inflammation. In conclusion, LLLI may have an anti-inflammatory effect on HGFs in a high glucose environment and may benefit the treatment of periodontal disease in diabetes patients.
Keyphrases
- high glucose
- endothelial cells
- oxidative stress
- inflammatory response
- anti inflammatory
- diabetic rats
- poor prognosis
- type diabetes
- cardiovascular disease
- reactive oxygen species
- dna damage
- lps induced
- lipopolysaccharide induced
- newly diagnosed
- ejection fraction
- toll like receptor
- glycemic control
- patient reported outcomes
- signaling pathway
- genome wide
- immune response
- transcription factor
- dna methylation
- metabolic syndrome
- end stage renal disease
- mass spectrometry
- insulin resistance
- skeletal muscle
- patient reported
- endoplasmic reticulum stress
- induced pluripotent stem cells