Lim Wonbong, Lee SungGa, Kim Inae, Chung Mina, Kim Misook, Lim Hoisoon, Park Jinsoo, Kim Okjoon, Choi Hongran
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.
Lasers Surg Med. 2007 Aug;39(7):614-21. doi: 10.1002/lsm.20533.
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.
STUDY DESIGN/MATERIALS AND 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 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)).
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.
在特定的病理生理情况下，即炎症和氧化应激中，抑制环氧化酶（COX）和前列腺素E2（PGE2）可保护细胞免受损伤。尽管在临床领域已有报道称特定波长的照射在伤口愈合过程中具有抗炎作用，但其生理机制尚未阐明。本研究的目的是探究与现有COX抑制剂相比，635纳米发光二极管（LED）照射的抗炎机制。
研究设计/材料与方法：本研究探讨了635纳米照射对花生四烯酸（AA）处理的人牙龈成纤维细胞（hGF）中PGE2释放、COX和磷脂酶A2（PLA2）表达以及活性氧（ROS）解离的抗炎作用。将这些结果与现有的COX抑制剂吲哚美辛和布洛芬进行比较。通过酶免疫测定法测量PGE2释放，通过蛋白质印迹法和逆转录聚合酶链反应（RT-PCR）测量COX表达，通过流式细胞术、激光扫描共聚焦显微镜和RT-PCR测量ROS水平。
结果表明，635纳米照射和现有COX抑制剂均抑制COX表达和PGE2释放。与吲哚美辛和布洛芬不同，635纳米照射可导致ROS水平以及胞质磷脂酶A2（cPLA2）和分泌型磷脂酶A2（sPLA2）的mRNA表达降低。
综上所述，与吲哚美辛和布洛芬不同，635纳米照射可直接使ROS解离。这抑制了cPLA2、sPLA2和COX的表达，并导致PGE2释放受到抑制。因此，我们认为635纳米照射像COX抑制剂一样抑制PGE2合成，似乎可作为一种抗炎工具。
