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光生物调节(450nm)通过 ROS/MAPK/mTOR 信号通路改变牙周炎细菌的感染。

Photobiomodulation (450 nm) alters the infection of periodontitis bacteria via the ROS/MAPK/mTOR signaling pathway.

机构信息

Department of Stomatology, China-Japan Union Hospital of Jilin University, Changchun, 130033, China.

Department of Breast Surgery, China-Japan Union Hospital of Jilin University, Changchun, 130033, China.

出版信息

Free Radic Biol Med. 2020 May 20;152:838-853. doi: 10.1016/j.freeradbiomed.2020.01.184. Epub 2020 Jan 31.

DOI:10.1016/j.freeradbiomed.2020.01.184
PMID:32014500
Abstract

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 HO (a biomarker of oxidative stress) and the free radicals (NO and O) 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.

摘要

我们旨在研究光生物调节(PBM)对牙周炎的影响。通过牙龈卟啉单胞菌感染比格犬建立牙周炎模型。拔牙后立即切除下颌第二和第三前磨牙,并放置植入物。左侧牙龈接受 PBM(450nm)照射作为 LG 组,右侧未照射作为 CG(对照)组。PBM 治疗通过增加活性氧(ROS)和活性氮(RNS)的水平来增加氧化应激。HO(氧化应激的生物标志物)和自由基(NO 和 O)水平升高,降低了优势病原体的浓度,并通过影响 p-AMPK、Runt 相关转录因子 2(RUNX2)、p-c-Jun N-末端激酶(JNK)/哺乳动物雷帕霉素靶蛋白(mTOR)和乙酰辅酶 A 羧化酶 1(ACC1)来调节 ROS/RNS/AMP 激活蛋白激酶(AMPK)/mTOR 通路。PBM 治疗增加了唾液中白细胞介素 1 受体拮抗剂(IL-1ra)、白细胞介素(IL)-10、总抗氧化能力(TAC)和过氧化氢酶(CAT)的水平,降低了肿瘤坏死因子(TNF)α和白细胞介素(IL)-1β、丙二醛(MDA)和 8-羟基脱氧鸟苷(8-OHdG)的水平(p<0.05)。所有结果都有助于预防牙周炎感染。PBM 治疗通过控制优势病原体的侵袭,通过影响 ROS/RNS/AMPK/mTOR 信号通路来调节唾液抗炎和抗氧化防御,从而改善骨密度和种植体骨整合。

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