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掺钕钇铝石榴石激光照射通过人牙髓细胞中的p38丝裂原活化蛋白激酶途径消除了肽聚糖引起的白细胞介素-6水平升高。

Neodymium-doped yttrium-aluminium-garnet laser irradiation abolishes the increase in interleukin-6 levels caused by peptidoglycan through the p38 mitogen-activated protein kinase pathway in human pulp cells.

作者信息

Shiba Hideki, Tsuda Hidehiro, Kajiya Mikihito, Fujita Tsuyoshi, Takeda Katsuhiro, Hino Takamune, Kawaguchi Hiroyuki, Kurihara Hidemi

机构信息

Department of Periodontal Medicine, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan.

出版信息

J Endod. 2009 Mar;35(3):373-6. doi: 10.1016/j.joen.2008.11.028.

Abstract

The anti-inflammatory effects of low-power laser irradiation have previously been reported. However, how the laser irradiation regulates the expression of inflammatory cytokines remains unknown. In the present study, to elucidate the mechanism behind the anti-inflammatory effect, we examined the effects of low-power neodymium-doped yttrium-aluminium-garnet (Nd:YAG) laser irradiation on interleukin (IL)-6 expression in human pulp (HP) cells stimulated by peptidoglycan (PGN) and focused on intracellular signaling pathways. Low-power Nd:YAG laser irradiation obviated the PGN-induced increase in IL-6 levels in HP cells. A p38 mitogen-activated protein kinase inhibitor, SB203580, also inhibited the increase in IL-6 messenger RNA levels. PGN stimulated the activity of phosphorylated p38 in HP cells. Low-power laser irradiation inhibited the activity. Thus, suppression of the phosphorylated p38 activity by low-power laser irradiation in HP cells culminates in inhibition of the increase in IL-6 induced by PGN, suggesting that low-power laser irradiation regulates intracellular signaling molecule activities to exert its anti-inflammatory effect.

摘要

低功率激光照射的抗炎作用此前已有报道。然而,激光照射如何调节炎性细胞因子的表达仍不清楚。在本研究中,为阐明抗炎作用背后的机制,我们检测了低功率掺钕钇铝石榴石(Nd:YAG)激光照射对肽聚糖(PGN)刺激的人牙髓(HP)细胞中白细胞介素(IL)-6表达的影响,并聚焦于细胞内信号通路。低功率Nd:YAG激光照射消除了PGN诱导的HP细胞中IL-6水平的升高。p38丝裂原活化蛋白激酶抑制剂SB203580也抑制了IL-6信使核糖核酸水平的升高。PGN刺激了HP细胞中磷酸化p38的活性。低功率激光照射抑制了该活性。因此,低功率激光照射对HP细胞中磷酸化p38活性的抑制最终导致对PGN诱导的IL-6升高的抑制,这表明低功率激光照射通过调节细胞内信号分子活性来发挥其抗炎作用。

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