安普克
SIRT3
SOD2
氧化应激
炎症
化学
蛋白激酶A
AMP活化蛋白激酶
细胞生物学
磷酸化
医学
免疫学
锡尔图因
超氧化物歧化酶
生物化学
生物
乙酰化
基因
作者
Haizheng Zhang,Chenyi Zhang,Lai Pan,Yifan Chen,Zirui Bian,Yihong Yang,Ke Tang,Weilian Sun,Lili Chen,Jingyi Tan
标识
DOI:10.1016/j.jphotobiol.2024.112845
摘要
Photobiomodulation is extensively employed in the management of chronic inflammatory diseases such as periodontitis because of its anti-inflammatory and antioxidant effects. This study used low-level Nd:YAG laser to investigate the mechanism of photobiomodulation as well as the role of adenosine monophosphate-activated protein kinase (AMPK) and Sirtuins (SIRT) 3 in it, providing new clues for the treatment of periodontitis.Human gingival fibroblasts (HGFs) were extracted from gingiva and stimulated with LPS. The suitable parameters of Nd:YAG laser were chosen for subsequent experiments by detecting cell viability. We assessed the level of inflammation and oxidative stress as well as AMPK and SIRT3. The mechanism for AMPK targeting SIRT3 modulating the anti-inflammatory and antioxidant effects of photobiomodulation was explored by the AMPK inhibitor (Compound C) test, cell transfection, western blot, and immunofluorescence.HGFs were isolated and identified, followed by the identification of optimal Nd:YAG laser parameters (60 mJ, 15 Hz, 10s) for subsequent experimentation. With this laser, inflammatory factors (IL-6, TNF-α, COX2, and iNOS) decreased as well as the phosphorylation and nuclear translocation of NFκB-P65. SOD2 was up-regulated but reactive oxygen species (ROS) was down-regulated. The laser treatment exhibited enhancements in AMPK phosphorylation and SIRT3 expression. The above effects could all be reversed by Compound C. Silencing AMPK or SIRT3 by siRNA, the down-regulation of COX2, iNOS, and ROS by laser was inhibited. SIRT3 was down-regulated when the AMPK was silenced.Low-level Nd:YAG laser activated AMPK-SIRT3 signaling pathway, facilitating the anti-inflammatory and antioxidative activity.
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