Low-level Er:YAG laser irradiation enhances osteoblast proliferation through activation of MAPK/ERK
Low-level Er:YAG laser irradiation enhances osteoblast proliferation through activation of MAPK/ERK
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DOI：
10.1007/s10103-010-0761-5
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发表时间：
2010-07-01
影响因子：
2.1
通讯作者：
Izumi, Yuichi
中科院分区：
文献类型：
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作者：
Aleksic, Verica;Aoki, Akira;Izumi, Yuichi
尽管高强度Er:YAG激光照射在牙周和种植体周围治疗中的应用不断增加，但低强度Er:YAG激光对周围组织和细胞的影响仍不清楚。在本研究中，研究了低水平Er:YAG激光照射对成骨细胞增殖的影响。成骨细胞系 MC3T3-E1 的细胞采用低水平 Er:YAG 激光照射和各种激光设置组合（注量 0.7-17.2 J/cm(2)）以及照射期间不存在或存在培养基的情况进行处理。在第1天和/或第3天，通过细胞计数和乳酸脱氢酶(LDH)水平的测量来确定细胞增殖和死亡。此外，通过抑制 MAPK 途径，然后通过蛋白质印迹测量 MAPK 磷酸化，研究了丝裂原激活蛋白激酶 (MAPK) 途径在激光增强细胞增殖中的作用。在第 1 天和第 3 天，各种照射参数组合的增殖率均较高。在能量密度约为 1.0-15.1 J/cm(2) 的激光照射的 MC3T3-E1 细胞中也观察到显着较高的增殖率，但未观察到 LDH 活性增加。此外，低水平 Er:YAG 照射在照射后 5 至 30 分钟诱导细胞外信号调节蛋白激酶 (MAPK/ERK) 磷酸化。尽管 MAPK/ERK 1/2 抑制剂 U0126 显着抑制激光增强的细胞增殖，但未明确检测到应激激活蛋白激酶/Jun N 末端激酶 (SAPK/JNK) 和 p38 MAPK 的激活。这些结果表明，低水平Er:YAG激光照射主要通过激活MAPK/ERK来增加成骨细胞增殖，这表明Er:YAG激光可能能够促进牙周和种植体周围治疗后的骨愈合。
Although the use of high-level Er:YAG laser irradiation has been increasing in periodontal and peri-implant therapy, the effects of low-level Er:YAG laser on surrounding tissues and cells remain unclear. In the present study, the effects of low-level Er:YAG laser irradiation on osteoblast proliferation were investigated. Cells of the osteoblastic cell line MC3T3-E1 were treated with low-level Er:YAG laser irradiation with various combinations of laser settings (fluence 0.7-17.2 J/cm(2)) and in the absence or presence of culture medium during irradiation. On day 1 and/or day 3, cell proliferation and death were determined by cell counting and by measurement of lactate dehydrogenase (LDH) levels. Further, the role of mitogen-activated protein kinase (MAPK) pathways in laser-enhanced cell proliferation was investigated by inhibiting the MAPK pathways and then measuring MAPK phosphorylation by Western blotting. Higher proliferation rates were found with various combinations of irradiation parameters on days 1 and 3. Significantly higher proliferation was also observed in laser-irradiated MC3T3-E1 cells at a fluence of approximately 1.0-15.1 J/cm(2), whereas no increase in LDH activity was observed. Further, low-level Er:YAG irradiation induced the phosphorylation of extracellular signal-regulated protein kinase (MAPK/ERK) 5 to 30 min after irradiation. Although MAPK/ERK 1/2 inhibitor U0126 significantly inhibited laser-enhanced cell proliferation, activation of stress-activated protein kinases/Jun N-terminal kinase (SAPK/JNK) and p38 MAPK was not clearly detected. These results suggest that low-level Er:YAG laser irradiation increases osteoblast proliferation mainly by activation of MAPK/ERK, suggesting that the Er:YAG laser may be able to promote bone healing following periodontal and peri-implant therapy.