The anti-inflammatory mechanism of 635 nm light-emitting-diode irradiation compared with existing COX inhibitors.
OBJECTIVE
Inhibition of cyclooxygenase (COX) and prostaglandin E(2) (PGE(2)) protects cells against cell injury in specific pathophysiological situations: inflammation and oxidative stress. Although the anti-inflammatory effects have been reported in clinical fields for specific wavelength irradiation during wound healing, the physiological mechanism has not been clarified yet. The aim of the present study is to investigate the anti-inflammatory mechanism of 635 nm light-emitting-diode (LED) irradiation compared with existing COX inhibitors.


METHODS
The present study investigated anti-inflammatory effects of 635 nm irradiation on PGE(2) release, COX and phospholipase A(2) (PLA(2)) expression, and reactive oxygen species (ROS) dissociation in arachidonic acid (AA)-treated human gingival fibroblast (hGF). These results were compared with their existing COX inhibitors: indomethacin and ibuprofen. The PGE(2) release was measured by enzyme immunoassay, the COX expression was measured by western blot and reverse transcriptase polymerase chain reaction (RT-PCR), and ROS level was measured by flow cytometry, laser scanning confocal microscope and RT-PCR.


RESULTS
Results showed that 635 nm irradiation and existing COX inhibitors inhibit expression of COX and PGE(2) release. Unlike indomethacin and ibuprofen, 635 nm irradiation leads to a decrease of ROS levels and mRNA expression of cytosolic phospholipase A(2) (cPLA(2)) and secretary phospholipase A(2) (sPLA(2)).


CONCLUSIONS
Taken together, 635 nm irradiation, unlike indomethacin and ibuprofen, can directly dissociate the ROS. This inhibits cPLA(2), sPLA(2), and COX expression, and results in the inhibition of PGE(2) release. Thus, we suggest that 635 nm irradiation inhibits PGE(2) synthesis like COX inhibitor and appears to be useful as an anti-inflammatory tool.
Lim
Wonbong
W
Department of Oral Pathology, 2nd Stage of Brain Korea 21 for School of Dentistry, Dental Science Research Institute, Chonnam National University, Bug-Gu, Gwangju, Korea.
Lee
SungGa
S
Kim
Inae
I
Chung
Mina
M
Kim
Misook
M
Lim
Hoisoon
H
Park
Jinsoo
J
Kim
Okjoon
O
Choi
Hongran
H
D000328:Adult; D015415:Biomarkers; D015153:Blotting, Western; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use*; D015232:Dinoprostone / Q000096:biosynthesis / Q000235:genetics; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects; D005434:Flow Cytometry; D005882:Gingival Diseases / Q000188:drug therapy* / Q000473:pathology / Q000532:radiotherapy*; D006801:Humans; D007052:Ibuprofen / Q000627:therapeutic use; D007213:Indomethacin / Q000627:therapeutic use; D018613:Microscopy, Confocal; D018384:Oxidative Stress / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects; D010789:Phototherapy / Q000379:methods*; D011451:Prostaglandin-Endoperoxide Synthases / Q000096:biosynthesis / Q000235:genetics; D012313:RNA / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014945:Wound Healing / Q000187:drug effects / Q000528:radiation effects
D015415:Biomarkers; D016861:Cyclooxygenase Inhibitors; D017382:Reactive Oxygen Species; D012313:RNA; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; D007052:Ibuprofen; D007213:Indomethacin