氧化应激
牙周炎
牙龈卟啉单胞菌
PI3K/AKT/mTOR通路
活性氧
化学
安普克
丙二醛
超氧化物歧化酶
运行x2
过氧化氢酶
MAPK/ERK通路
药理学
激酶
蛋白激酶A
信号转导
医学
内科学
成骨细胞
生物化学
体外
作者
Hui Li,Tong Sun,Cong Liu,Yan Cao,Xin Liu
标识
DOI:10.1016/j.freeradbiomed.2020.01.184
摘要
We aimed to investigate the effects of photobiomodulation (PBM) on periodontitis. A periodontitis model was established via Porphyromonas gingivalis infection in beagles. Mandibular second and third premolars were removed, and implants were positioned immediately after tooth extraction. Left gingiva was irradiated with PBM (450 nm) as the LG group, and right side without irradiation was regarded as the CG (control) group. PBM treatment increased oxidative stress by increasing the levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS). The elevated levels of H2O2 (a biomarker of oxidative stress) and the free radicals (NO• and O2•-) reduced the concentration of dominant pathogens and regulated ROS/RNS/AMP-activated protein kinase (AMPK)/mTOR pathway by affecting p-AMPK, Runt-related transcription factor 2 (RUNX2), p-c-Jun N-terminal kinase (JNK)/mammalian target of rapamycin (mTOR), and acetyl-CoA carboxylase 1 (ACC1). PBM therapy increased salivary levels of interleukin-1 receptor antagonist (IL-1ra), interleukin (IL)-10, total antioxidant capacity (TAC) and catalase (CAT), and reduced the levels of tumor necrosis factor (TNF)α and interleukin (IL)-1β, malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) (p < 0.05). All the results contributed to preventing periodontitis infection. PBM therapy improved bone mineral density and implant osseointegration by controlling dominant pathogens invasion via the upregulation of salivary anti-inflammatory and antioxidant defense by affecting ROS/RNS/AMPK/mTOR signaling pathway.
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