Department of Oral Pathology, 2nd stage of Brain Korea 21 for School of Dentistry, Dental Science Research Institute, Chonnam National University, Bug-Gu, Gwangju, 500-757, Korea.
Lasers Med Sci. 2012 Mar;27(2):459-67. doi: 10.1007/s10103-011-0971-5. Epub 2011 Aug 4.
Human gingival fibroblasts (hGFs) play an important role in the inflammatory reaction to lipopolysaccharide (LPS) from P. gingivalis, which infects periodontal connective tissue. In addition, although light-emitting diode (LED) irradiation has been reported to have biostimulatory effects, including anti-inflammatory activity, the pathological mechanisms of these effects are unclear. This study examined the effects of 635-nm irradiation of P. gingivalis LPS-treated human gingival fibroblasts on inflammatory cytokine profiles and the mitogen-activated protein kinase (MAPK) pathway, which is involved in cytokine production. Gingival fibroblasts treated or not treated with P. gingivalis LPS were irradiated with 635-nm LED light, and cytokine profiles in the supernatant were assessed using a human inflammation antibody array. Expression of cyclooxyginase-2 (COX-2) protein and phosphorylation of extracellular signal-regulated kinase (ERK 1/2), p38, and c-Jun-N-terminal kinase (JNK) were assessed by Western-blot analysis to determine the effects on the MAPK pathway, and prostaglandin E(2) (PGE(2)) in the supernatant was measured using an enzyme-linked immunoassay. COX-2 protein expression and PGE(2) production were significantly increased in the LPS-treated group and decreased by LED irradiation. LPS treatment of gingival fibroblasts led to the increased release of the pro-inflammatory-related cytokines interleukin-6 (IL-6) and IL-8, whereas LED irradiation inhibited their release. Analysis of MAPK signal transduction revealed a considerable decrease in p38 phosphorylation in response to 635-nm radiation either in the presence or absence of LPS. In addition, 635-nm LED irradiation significantly promoted JNK phosphorylation in the presence of LPS. LED irradiation can inhibit activation of pro-inflammatory cytokines, mediate the MAPK signaling pathway, and may be clinically useful as an anti-inflammatory tool.
人牙龈成纤维细胞（hGFs）在牙龈卟啉单胞菌（P. gingivalis）脂多糖（LPS）引起的牙周组织炎症反应中发挥重要作用。此外，虽然已经报道了发光二极管（LED）照射具有生物刺激作用，包括抗炎活性，但这些作用的病理机制尚不清楚。本研究探讨了 635nm 照射牙龈卟啉单胞菌 LPS 处理的人牙龈成纤维细胞对炎症细胞因子谱和丝裂原激活蛋白激酶（MAPK）通路的影响，该通路参与细胞因子的产生。用或不用牙龈卟啉单胞菌 LPS 处理的牙龈成纤维细胞用 635nm LED 光照射，并使用人炎症抗体阵列评估上清液中的细胞因子谱。通过 Western-blot 分析评估环氧化酶-2（COX-2）蛋白的表达和细胞外信号调节激酶（ERK 1/2）、p38 和 c-Jun-N-末端激酶（JNK）的磷酸化，以确定对 MAPK 通路的影响，并使用酶联免疫吸附测定法测量上清液中的前列腺素 E（2）（PGE（2））。LPS 处理组中 COX-2 蛋白表达和 PGE（2）产生明显增加，而 LED 照射则减少。LPS 处理牙龈成纤维细胞导致促炎相关细胞因子白细胞介素-6（IL-6）和 IL-8 的释放增加，而 LED 照射抑制其释放。MAPK 信号转导分析显示，在存在或不存在 LPS 的情况下，635nm 辐射导致 p38 磷酸化明显减少。此外，在 LPS 存在的情况下，635nm LED 照射显著促进了 JNK 磷酸化。LED 照射可抑制促炎细胞因子的激活，调节 MAPK 信号通路，并且可能在临床上用作抗炎工具。
