photobiomodulation (PBM)

  • 文章类型: Journal Article
    目前,慢性阻塞性肺疾病(COPD)对全球发病率和死亡率有很大影响。CD4+的增加,CD8+细胞表达NF-κB,STAT4、IFN-γ和穿孔素与吸烟习惯有关,吸烟史,气流速率,阻塞和肺气肿。此外,CD4+CD25+Foxp3+调节性T细胞(Tregs)的缺乏可能损害免疫系统的正常功能并导致呼吸道免疫性疾病。另一方面,由Treg细胞和巨噬细胞产生的抗炎细胞因子IL-10,抑制在COPD中表达的几种促炎细胞因子的合成。因此,免疫治疗策略,如光生物调节(PBM),旨在调节细胞因子的水平,COPD的趋化因子和转录因子。因此,这项研究的目的是评估COPD小鼠模型中PBM治疗后肺中CD4STAT4和CD4CD25Foxp3细胞以及CD4IFN-γ和CD4CD25IL-10的产生。
    我们通过气管应用香烟烟雾提取物在C57BL/6小鼠中诱导COPD。应用PMB治疗整个7周,收集支气管肺泡灌洗(BAL)和肺以研究肺中IFN-γ和IL-10的产生。最后一次服用香烟烟雾提取物后(7周结束),24小时后,动物被安乐死。单因素方差分析和NewmanKeuls检验用于统计学分析,显著性水平调整至5%(p<0.05)。
    该结果表明PBM改善了COPD症状,减少炎症细胞的数量(巨噬细胞,中性粒细胞和淋巴细胞),IFN-γ的水平,IL-10增加。我们还观察到胶原蛋白的减少,粘液,支气管收缩指数,肺泡肿大,CD4+,CD8+,CD4+STAT4+,和CD4+IFN-γ+细胞。此外,在治疗组中,我们发现CD4+CD25+Foxp3+和CD4+IL-10+T细胞增加。
    本研究提示PBM治疗可作为COPD的免疫治疗策略。
    UNASSIGNED: Currently, Chronic Obstructive Pulmonary Disease (COPD) has a high impact on morbidity and mortality worldwide. The increase of CD4+, CD8+ cells expressing NF-κB, STAT4, IFN-γ and perforin are related to smoking habit, smoking history, airflow rate, obstruction and pulmonary emphysema. Furthermore, a deficiency in CD4+CD25+Foxp3+ regulatory T cells (Tregs) may impair the normal function of the immune system and lead to respiratory immune disease. On the other hand, the anti-inflammatory cytokine IL-10, produced by Treg cells and macrophages, inhibits the synthesis of several pro-inflammatory cytokines that are expressed in COPD. Therefore, immunotherapeutic strategies, such as Photobiomodulation (PBM), aim to regulate the levels of cytokines, chemokines and transcription factors in COPD. Consequently, the objective of this study was to evaluate CD4+STAT4 and CD4+CD25+Foxp3+ cells as well as the production of CD4+IFN- γ and CD4+CD25+IL-10 in the lung after PBM therapy in a COPD mice model.
    UNASSIGNED: We induced COPD in C57BL/6 mice through an orotracheal application of cigarette smoke extract. PMB treatment was applied for the entire 7 weeks and Bronchoalveolar lavage (BAL) and lungs were collected to study production of IFN- γ and IL-10 in the lung. After the last administration with cigarette smoke extract (end of 7 weeks), 24 h later, the animals were euthanized. One-way ANOVA followed by NewmanKeuls test were used for statistical analysis with significance levels adjusted to 5% (p < 0.05).
    UNASSIGNED: This result showed that PBM improves COPD symptomatology, reducing the number of inflammatory cells (macrophages, neutrophils and lymphocytes), the levels of IFN-γ among others, and increased IL-10. We also observed a decrease of collagen, mucus, bronchoconstriction index, alveolar enlargement, CD4+, CD8+, CD4+STAT4+, and CD4+IFN-γ+ cells. In addition, in the treated group, we found an increase in CD4+CD25+Foxp3+ and CD4+IL-10+ T cells.
    UNASSIGNED: This study suggests that PBM treatment could be applied as an immunotherapeutic strategy for COPD.
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  • 文章类型: Journal Article
    研究了同时应用叔丁基过氧化氢(tBHP)和多色近红外(NIR)辐射对牛血的影响,以确定NIR光是否降低红细胞(RBC)对氧化应激的敏感性。该研究评估了各种暴露方法,波长范围,和光学滤波类型。连续NIR暴露显示无细胞血红蛋白变化的双相反应,在低通量下观察到抗氧化作用,在较高通量下观察到有害作用。最佳暴露持续时间在60s至15分钟之间。还在750-1100nm范围内的波长范围内测试了保护效果,所有这些都减少了溶血,特别是在750nm,875nm,和900纳米。比较宽带NIR和远红光(750nm)显示溶血减少没有显著差异。脉冲剂量的近红外辐射允许安全增加辐射剂量,在持续暴露有害的较高剂量下有效限制溶血。这些发现强调了NIR光生物调节在保护红细胞免受氧化应激方面的潜力,并将有助于新型医疗治疗设备的有效设计。
    The effect of simultaneous application of tert-butyl hydroperoxide (tBHP) and polychromatic near-infrared (NIR) radiation on bovine blood was examined to determine whether NIR light decreases the susceptibility of red blood cells (RBCs) to oxidative stress. The study assessed various exposure methods, wavelength ranges, and optical filtering types. Continuous NIR exposure revealed a biphasic response in cell-free hemoglobin changes, with antioxidative effects observed at low fluences and detrimental effects at higher fluences. Optimal exposure duration was identified between 60 s and 15 min. Protective effects were also tested across wavelengths in the range of 750-1100 nm, with all of them reducing hemolysis, notably at 750 nm, 875 nm, and 900 nm. Comparing broadband NIR and far-red light (750 nm) showed no significant difference in hemolysis reduction. Pulse-dosed NIR irradiation allowed safe increases in radiation dose, effectively limiting hemolysis at higher doses where continuous exposure was harmful. These findings highlight NIR photobiomodulation\'s potential in protecting RBCs from oxidative stress and will be helpful in the effective design of novel medical therapeutic devices.
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  • 文章类型: Journal Article
    阿尔茨海默病(AD)是一个重大的公共卫生问题,影响着全世界数百万人。尽管对AD的治疗策略进行了数十年的研究,这种破坏性疾病的有效预防或治疗仍然难以捉摸。在这次审查中,我们讨论了光生物调节(PBM)预防和缓解AD相关病理的潜力,专注于这种疗法的生物学机制。还强调了这种非侵入性和非药物治疗的未来研究方向和临床实践指导。现有证据表明,不同的治疗模式,包括经颅和全身PBM,以及最近提出的远程PBM,对于AD来说,一切都可能是有希望的。PBM发挥不同的生物学效应,比如增强线粒体功能,减轻由激活的神经胶质细胞引起的神经炎症,增加脑灌注,改善淋巴引流,调节肠道微生物组,促进Myokine生产,和调节免疫系统。我们建议PBM可以作为AD的有效治疗干预。
    Alzheimer\'s disease (AD) poses a significant public health problem, affecting millions of people across the world. Despite decades of research into therapeutic strategies for AD, effective prevention or treatment for this devastating disorder remains elusive. In this review, we discuss the potential of photobiomodulation (PBM) for preventing and alleviating AD-associated pathologies, with a focus on the biological mechanisms underlying this therapy. Future research directions and guidance for clinical practice for this non-invasive and non-pharmacological therapy are also highlighted. The available evidence indicates that different treatment paradigms, including transcranial and systemic PBM, along with the recently proposed remote PBM, all could be promising for AD. PBM exerts diverse biological effects, such as enhancing mitochondrial function, mitigating the neuroinflammation caused by activated glial cells, increasing cerebral perfusion, improving glymphatic drainage, regulating the gut microbiome, boosting myokine production, and modulating the immune system. We suggest that PBM may serve as a powerful therapeutic intervention for AD.
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  • 文章类型: Journal Article
    延长的内质网(ER)应激有助于细胞凋亡并干扰骨稳态。虽然光生物调节(PBM)可用于内质网应激诱导的疾病,PBM在缓解细胞凋亡中的作用尚不清楚。在ER压力期间,糖原合成酶激酶-3β(GSK-3β)是关键的;然而,其在PBM中的功能仍不确定。因此,本研究旨在探讨GSK-3β在625nm发光二极管照射(LEDI)减轻衣霉素(TM)诱导的细胞凋亡中的作用。根据结果,通过ROS产生pre-625nmLEDI(Pre-IR)磷酸化GSK-3β。与TM组相比,Pre-IR+TM组通过调节GSK-3β降低真核翻译起始因子2(eIF-2α)α亚基的磷酸化和B细胞淋巴瘤蛋白2(Bcl-2)相关X(Bax)/Bcl-2比值。此外,在防止TM诱导的早期和晚期细胞凋亡方面,在Pre-IR+TM和Pre-LiCl+TM组之间观察到相似的趋势。总之,这项研究表明,在TM诱导的ER应激中,Pre-IR处理有利于通过GSK-3β磷酸化防止细胞凋亡。
    Prolonged endoplasmic reticulum (ER) stress contributes to cell apoptosis and interferes with bone homeostasis. Although photobiomodulation (PBM) might be used for ER stress-induced diseases, the role of PBM in relieving cell apoptosis remains unknown. During ER stress, glycogen synthase kinase-3β (GSK-3β) is critical; however, its functions in PBM remain uncertain. Thus, this study aimed to investigate the role of GSK-3β in 625 nm light-emitting diode irradiation (LEDI) relieving tunicamycin (TM)-induced apoptosis. Based on the results, pre-625 nm LEDI (Pre-IR) phosphorylated GSK-3β via ROS production. Compared with the TM group, Pre-IR + TM group reduced the phosphorylation of the α-subunit of eukaryotic translation initiation factor 2 (eIF-2α) and B-cell lymphoma protein 2 (Bcl-2)-associated X (Bax)/Bcl-2 ratio through regulating GSK-3β. Furthermore, a similar tendency was observed between Pre-IR + TM and Pre-LiCl+TM groups in preventing TM-induced early and late apoptosis. In summary, this study suggests that the Pre-IR treatment in TM-induced ER stress is beneficial for preventing cell apoptosis via GSK-3β phosphorylation.
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  • 文章类型: Journal Article
    全球,骨质疏松症是最主要的退行性骨病。使用脂肪间充质干细胞(ADMSCs)的干细胞再生疗法是一种有前途的骨质疏松症治疗途径。光生物调节(PBM)由于其增强干细胞增殖和分化特性的能力而引起了相当大的国际吸引力。此外,已使用成骨分化诱导剂和PBM的组合建立了ADMSCs向成骨细胞的分化和细胞增殖作用。这项体外研究应用了地塞米松,β-甘油磷酸二钠,和抗坏血酸作为成骨诱导分化培养基的分化诱导剂。此外,PBM在825nm的近红外(NIR)波长下,绿色(G)波长为525nm,并且使用5J/cm2的单一注量将这两种波长的新组合应用于刺激永生化ADMSCs向早期成骨细胞的增殖和分化效力。流式细胞术和ELISA用于使用早期和晚期成骨细胞蛋白标志物鉴定成骨细胞抗原。采用茜素红染色来鉴定培养物中细胞的富含钙的沉积物。检查细胞的形态,和生化测定,如EdU增殖测定,MTT增殖和活力测定,线粒体膜电位测定,并进行了活性氧分析。中央划痕测试确定了细胞的运动潜力。研究结果表明,PBM治疗和成骨分化诱导剂的组合刺激了永生化ADMSCs的有希望的早期成骨分化。在选定的试验中,NIR-GreenPBM组合似乎为永生化ADMSC分化为早期成骨细胞提供了巨大的潜力。然而,需要进一步的研究来确定这种新型波长组合的有效性。这项研究有助于知识体系,并有助于建立使用PBM的体外成骨分化标准。
    Worldwide, osteoporosis is the utmost predominant degenerative bone condition. Stem cell regenerative therapy using adipose-derived mesenchymal stem cells (ADMSCs) is a promising therapeutic route for osteoporosis. Photobiomodulation (PBM) has sparked considerable international appeal due to its\' ability to augment stem cell proliferation and differentiation properties. Furthermore, the differentiation of ADMSCs into osteoblast cells and cellular proliferation effects have been established using a combination of osteogenic differentiation inducers and PBM. This in vitro study applied dexamethasone, β-glycerophosphate disodium, and ascorbic acid as differentiation inducers for osteogenic induction differentiation media. In addition, PBM at a near-infrared (NIR) wavelength of 825 nm, a green (G) wavelength of 525 nm, and the novel combination of both these wavelengths using a single fluence of 5 J/cm2 had been applied to stimulate proliferation and differentiation effectivity of immortalised ADMSCs into early osteoblasts. Flow cytometry and ELISA were used to identify osteoblast antigens using early and late osteoblast protein markers. Alizarin red Stain was employed to identify calcium-rich deposits by cells within culture. The morphology of the cells was examined, and biochemical assays such as an EdU proliferation assay, MTT proliferation and viability assay, Mitochondrial Membrane Potential assay, and Reactive Oxygen Species assay were performed. The Central Scratch Test determined the cells\' motility potential. The investigative outcomes revealed that a combination of PBM treatment and osteogenic differentiation inducers stimulated promising early osteogenic differentiation of immortalised ADMSCs. The NIR-Green PBM combination did appear to offer great potential for immortalised ADMSC differentiation into early osteoblasts amongst selected assays, however, further investigations will be required to establish the effectivity of this novel wavelength combination. This research contributes to the body of knowledge and assists in the establishment of a standard for osteogenic differentiation in vitro utilising PBM.
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  • 文章类型: English Abstract
    背景:评估光生物调节(PBM)治疗的当前和潜在适应症及其在预防或治疗与肿瘤治疗相关的副作用方面的证据水平(放射治疗,在最小程度上有利于造血干细胞移植)。并报告PBM治疗的推荐方式(参数和剂量)。
    方法:Embase,Medline/PubMed,科克伦,EBSCO,Scopus,和LILACS数据库进行了系统审查,以包括和分析评价PBM在预防或管理癌症治疗相关副作用方面的临床研究的出版物.使用的关键词是\“光生物调节\”;\“低水平激光治疗\”;\“急性口腔黏膜炎\”;\“急性吞咽困难\”;\“急性放射性皮炎\”;\“淋巴水肿\”;\“口干症\”;\“发育不良\”;\“下颌”;\“锁骨”“与神经放射病\”;包括前瞻性研究,而回顾性队列和非原始文章被排除在分析之外.
    结果:红色或红外光谱中的PBM在预防和管理某些与放疗有关的并发症的随机对照试验中已被证明是有效的,特别是急性粘膜炎,上皮膜炎和上肢淋巴水肿。与PBM相关的证据水平是异质的,但总体保持温和。主要限制是治疗方案的多样性和缺乏准确性,这可能会损害PBM结果的效率和可重复性。对于与化学/放射疗法相关的其他影响(味觉障碍,骨坏死,周围神经病变,脱发,掌足红感觉障碍)和造血干细胞移植(移植物抗宿主病),PBM的治疗缺乏研究或有限的研究,原因是证据水平减弱。然而,基于这些结果,有可能建立安全的实践参数和PBM剂量。
    结论:发表的数据表明,PBM本身可以被视为对接受放射治疗的患者的支持治疗,化疗,免疫疗法,激素治疗或靶向治疗,无论是在临床实践还是临床试验中。疗法。然而,直到关于其长期安全性的可靠数据公布,应谨慎考虑使用PBM,并在推荐的参数和剂量范围内,特别是在已知或可能的肿瘤区域进行。在这种情况下,应告知患者PBM的理论获益和风险,以便在治疗前获得知情同意.
    BACKGROUND: Assess the current and potential indications of photobiomodulation (PBM) therapy and their level of evidence in the prevention or treatment of side effects related to oncology treatments (radiation therapy, and to a minimal extent favored and hematopoietic stem cell transplants). And report on the recommended modalities (parameters and doses) of PBM therapy.
    METHODS: The Embase, Medline/PubMed, Cochrane, EBSCO, Scopus, and LILACS databases were systematically reviewed to include and analyze publications of clinical studies that evaluated PBM in the prevention or management side effects related to cancer treatments. The keywords used were \"photobiomodulation\"; \"low level laser therapy\"; \"acute oral mucositis\"; \"acute dysphagia\"; \"acute radiation dermatitis\"; \"lymphedema\"; \"xerostomia\"; \"dysgeusia\"; \"hyposalivation\"; \"lockjaw\"; \"bone necrosis\"; \"osteoradionecrosis\"; \"radiation induced fibrosis\"; \"voice and speech alterations\"; \"palmar-plantar erythrodysesthesia\"; \"graft versus host disease\"; \"peripheral neuropathy\"; \"chemotherapy induced alopecia\". Prospective studies were included, while retrospective cohorts and non-original articles were excluded from the analysis.
    RESULTS: PBM in the red or infrared spectrum has been shown to be effective in randomized controlled trials in the prevention and management of certain complications related to radiotherapy, in particular acute mucositis, epitheliitis and upper limb lymphedema. The level of evidence associated with PBM was heterogeneous, but overall remained moderate. The main limitations were the diversity and the lack of precision of the treatment protocols which could compromise the efficiency and the reproducibility of the results of the PBM. For other effects related to chemo/radiation therapy (dysgeusia, osteonecrosis, peripheral neuropathy, alopecia, palmar-plantar erythrodysaesthesia) and haematopoietic stem cell transplantation (graft versus host disease), treatment with PBM suffers from a lack of studies or limited studies at the origin of a weakened level of proof. However, based on these results, it was possible to establish safe practice parameters and doses of PBM.
    CONCLUSIONS: Published data suggest that PBM could therefore be considered as supportive care in its own right for patients treated with radiation, chemotherapy, immunotherapy, hormone therapy or targeted therapies, whether in clinical practice or clinical trials. therapies. However, until solid data have been published on its long-term safety, the use of PBM should be considered with caution and within the recommended parameters and doses, particularly when practiced in areas of known or possible tumours. In this case, the patient should be informed of the theoretical benefits and risks of PBM in order to obtain informed consent before treatment.
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  • 文章类型: Journal Article
    我们研究了使用发光二极管(led)640nm对谷氨酰胺依赖性CT26细胞进行光生物调节(PBM)的作用机制。将细胞暴露于0.147-10.979mW/cm2的640±15nm激光15分钟/天,持续10天。通过MTT(3-(4,5)-二甲基硫代偶氮(-z-y1)-3,5-二苯基四唑三胺)和膜联蛋白V-FITC测定法检测细胞增殖和凋亡。通过RT-PCR和Westernblotting检测细胞增殖相关基因的mRNA和蛋白水平,分别。使用Gln7.94mM,在第8天和第10天,谷氨酰胺成瘾基因GLUT1,MEK1,ERK2,BCL2,E2F1,HO-1,Ctnnb1和Per2显着上调(p<0.01)。在PBM治疗中,与非照明组相比,2.17mW/cm2可以显著减少细胞凋亡,mTOR1基因的mRNA水平显著上调,raptor的GLUT1和mTOR1,MEK1/2和ERK1/2的蛋白水平上调。LED640nm通过调节GLUT1,MEK/ERK,抑制细胞凋亡而不增加细胞增殖,和PI3K/AKT/mTOR信号。
    We investigated the mechanism of action of photobiomodulation (PBM) with light-emitting diode (led) 640 nm of glutamine-dependent CT26 cells. Cells were exposed to 0.147-10.979 mW/cm2 of 640 ± 15 nm laser light for 15 min/day for 10 days. Cell proliferation and apoptosis were detected by MTT (3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-diphenytetrazoliumromide) and annexin V-FITC assays. mRNA and protein levels of cell proliferation-related genes were measured by RT-PCR and western blotting, respectively. With Gln 7.94 mM, on Day 8 and 10, genes GLUT1, MEK1, ERK2, BCL2, E2F1, HO-1, Ctnnb1, and Per2 was significantly upregulated (p < 0.01) of glutamine addiction. In PBM therapy, compared with the non-illuminated group, 2.17 mW/cm2 can significantly reduce cell apoptosis, the mRNA level of gene mTOR1 was significantly upregulated, and the protein level of raptor of GLUT1 and mTOR1, MEK1/2, and ERK1/2 were upregulated. LED 640 nm inhibits cell apoptosis without increasing cell proliferation by regulating GLUT1, MEK/ERK, and PI3K/AKT/mTOR signals.
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  • 文章类型: Journal Article
    迫切需要可以预防或限制神经炎症过程并防止神经元变性的治疗方法。光生物调节(PBM),特定波长的光的治疗用途,是一种安全的方法,具有抗炎作用。本研究旨在评估PBM对LPS诱导的小鼠外周和中枢炎症的影响,以评估其作为抗炎治疗的潜力。每日,在LPS攻击之前,用红色/NIR光(RL)或具有40Hzγ频率闪烁的RL处理小鼠30分钟10天显示在脑中和全身的抗炎作用。PBM下调LPS诱导与炎症小体激活相关的关键促炎细胞因子,IL-1β和IL-18,并上调抗炎细胞因子,IL-10.RL提供了强大的抗炎作用,伽马闪烁的加入增强了这些效应。总的来说,这些结果证明了PBM作为通过细胞因子表达调节发挥作用的抗炎治疗的潜力.
    There is an urgent need for therapeutic approaches that can prevent or limit neuroinflammatory processes and prevent neuronal degeneration. Photobiomodulation (PBM), the therapeutic use of specific wavelengths of light, is a safe approach shown to have anti-inflammatory effects. The current study was aimed at evaluating the effects of PBM on LPS-induced peripheral and central inflammation in mice to assess its potential as an anti-inflammatory treatment. Daily, 30-min treatment of mice with red/NIR light (RL) or RL with a 40 Hz gamma frequency flicker for 10 days prior to LPS challenge showed anti-inflammatory effects in the brain and systemically. PBM downregulated LPS induction of key proinflammatory cytokines associated with inflammasome activation, IL-1β and IL-18, and upregulated the anti-inflammatory cytokine, IL-10. RL provided robust anti-inflammatory effects, and the addition of gamma flicker potentiated these effects. Overall, these results demonstrate the potential of PBM as an anti-inflammatory treatment that acts through cytokine expression modulation.
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  • 文章类型: Journal Article
    高频近红外(NIR)半导体激光照射对受压侧牙周膜区域的伤害性感受影响不明确,周围神经区域。本研究旨在研究近红外半导体激光辐照的影响,功率为120J,在ETM过程中,在压迫的牙周膜区诱导的炎性疼痛标志物和神经肽。近红外半导体激光器[910nm波长,45W最大输出功率,300mW平均输出功率,30kHz频率,和200ns脉冲宽度(Lumix2;Fisioline,Verduno,意大利)]被使用。在7周龄的Sprague-Dawley(280-300g)大鼠的上颌左侧第一磨牙和门牙上施加镍钛封闭线圈,产生50g的力,以诱导实验性牙齿移动(ETM)24小时。十只大鼠分为两组(ETM激光,n=5;ETM,n=5)。ETM组的右侧(即,未诱导ETM的一侧)作为未治疗组进行评估。我们进行了免疫荧光组织化学分析来定量白细胞介素(IL)-1β,环氧合酶-2(COX2),前列腺素E2(PGE2),和神经肽[降钙素基因相关肽(CGRP)]在牙周组织压缩区域的表达。使用事后Tukey-Kramer测试来比较各组。与ETM组相比,ETM+激光组显着抑制IL-1β(176.2±12.3vs.310.8±29.5;P<0.01),PGE2(104.4±14.34vs.329.6±36.52;P<0.01),和CGRP(36.8±4.88vs.78.0±7.13;P<0.01)表达。高频近红外半导体激光照射对ETM诱导的炎症有显著影响。高频近红外半导体激光照射可减轻正畸牙齿移动过程中的牙周炎症。
    High-frequency near-infrared (NIR) semiconductor laser-irradiation has an unclear effect on nociception in the compressed lateral periodontal ligament region, a peripheral nerve region. This study aimed to investigate the effects of NIR semiconductor laser irradiation, with a power of 120 J, on inflammatory pain markers and neuropeptides induced in the compressed lateral periodontal ligament area during ETM. A NIR semiconductor laser [910 nm wavelength, 45 W maximum output power, 300 mW average output power, 30 kHz frequency, and 200 ns pulse width (Lumix 2; Fisioline, Verduno, Italy)] was used. A nickel-titanium closed coil that generated a 50-g force was applied to the maxillary left-side first molars and incisors in 7-week-old Sprague-Dawley (280-300 g) rats to induce experimental tooth movement (ETM) for 24 h. Ten rats were divided into two groups (ETM + laser, n = 5; ETM, n = 5). The right side of the ETM group (i.e., the side without induced ETM) was evaluated as the untreated group. We performed immunofluorescent histochemistry analysis to quantify the interleukin (IL)-1β, cyclooxygenase-2 (COX2), prostaglandin E2 (PGE2), and neuropeptide [calcitonin gene-related peptide (CGRP)] expression in the compressed region of the periodontal tissue. Post-hoc Tukey-Kramer tests were used to compare the groups. Compared with the ETM group, the ETM + laser group showed significant suppression in IL-1β (176.2 ± 12.3 vs. 310.8 ± 29.5; P < 0.01), PGE2 (104.4 ± 14.34 vs. 329.6 ± 36.52; P < 0.01), and CGRP (36.8 ± 4.88 vs. 78.0 ± 7.13; P < 0.01) expression. High-frequency NIR semiconductor laser irradiation exerts significant effects on ETM-induced inflammation. High-frequency NIR semiconductor laser irradiation can reduce periodontal inflammation during orthodontic tooth movement.
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  • 文章类型: Journal Article
    理由:早期生活中的不良经历,包括虐待,创伤和忽视,与不良的身心健康结果有关。新出现的证据表明,那些经历过早期生活逆境(ELA)的人更有可能在成年期出现认知功能障碍和抑郁样症状。导致ELA负面后果的分子机制,然而,仍然不清楚。在缺乏有效管理选项的情况下,预期指导是ELA预防的主体。此外,没有可用的治疗方法可以预防或减轻ELA的神经系统后遗症,尤其是创伤压力。因此,本研究旨在探讨这些关联的机制,并评估光生物调节(PBM)一种非侵入性的治疗方法,可以防止ELA在以后的生活中的负面认知和行为表现。方法:从出生后第21至26天,通过反复的不可避免的电足电击诱导ELA。在最后一次电击后的第二天,每天2分钟的PBM治疗经颅连续7天。通过成年期的一系列行为测试来测量认知功能障碍和抑郁样行为。随后,少突胶质祖细胞(OPCs)分化,少突胶质细胞谱系细胞(OLs)的增殖和凋亡,成熟少突胶质细胞,髓鞘少突胶质细胞,氧化损伤的水平,活性氧(ROS)和总抗氧化能力的测量和分析使用免疫荧光染色,基于毛细管的免疫测定(ProteinSimple®)和抗氧化剂测定试剂盒。结果:暴露于ELA的大鼠表现出明显的少突胶质细胞功能障碍,包括减少OPCs的差异化,OLs的产生和存活减少,减少OL,成熟少突胶质细胞减少。此外,观察到髓鞘少突胶质细胞的缺陷,与氧化还原稳态失衡和累积的氧化损伤有关。这些变化伴随着认知功能障碍和抑郁样行为。重要的是,我们发现早期PBM治疗在很大程度上预防了这些病变,并逆转了ELA引起的神经系统后遗症.结论:总的来说,这些发现为ELA影响神经系统结局的机制提供了新的见解.此外,我们的研究结果支持PBM可能是预防ELA诱导的神经系统后遗症的一种有希望的策略。
    Rationale: Adverse experiences in early life including abuse, trauma and neglect, have been linked to poor physical and mental health outcomes. Emerging evidence implies that those who experienced early life adversity (ELA) are more likely to develop cognitive dysfunction and depressive-like symptoms in adulthood. The molecular mechanisms responsible for the negative consequences of ELA, however, remain unclear. In the absence of effective management options, anticipatory guidance is the mainstay of ELA prevention. Furthermore, there is no available treatment that prevents or alleviates the neurologic sequelae of ELA, especially traumatic stress. Hence, the present study aims to investigate the mechanisms for these associations and evaluate whether photobiomodulation (PBM), a non-invasive therapeutic procedure, can prevent the negative cognitive and behavioral manifestations of ELA in later life. Methods: ELA was induced by repeated inescapable electric foot shock of rats from postnatal day 21 to 26. On the day immediately following the last foot shock, 2-min daily PBM treatment was applied transcranially for 7 consecutive days. Cognitive dysfunction and depression-like behaviors were measured by a battery of behavioral tests in adulthood. Subsequently, oligodendrocyte progenitor cells (OPCs) differentiation, the proliferation and apoptosis of oligodendrocyte lineage cells (OLs), mature oligodendrocyte, myelinating oligodendrocyte, the level of oxidative damage, reactive oxygen species (ROS) and total antioxidant capacity were measured and analyzed using immunofluorescence staining, capillary-based immunoassay (ProteinSimple®) and antioxidant assay kit. Results: The rats exposed to ELA exhibited obvious oligodendrocyte dysfunction, including a reduction in OPCs differentiation, diminished generation and survival of OLs, decreased OLs, and decreased matured oligodendrocyte. Furthermore, a deficit in myelinating oligodendrocytes was observed, in conjunction with an imbalance in redox homeostasis and accumulated oxidative damage. These alternations were concomitant with cognitive dysfunction and depression-like behaviors. Importantly, we found that early PBM treatment largely prevented these pathologies and reversed the neurologic sequelae resulting from ELA. Conclusions: Collectively, these findings provide new insights into the mechanism by which ELA affects neurological outcomes. Moreover, our findings support that PBM may be a promising strategy to prevent ELA-induced neurologic sequelae that develops later in life.
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