The Influence of Light on Reactive Oxygen Species and NF-кB in Disease Progression

Rajendran, Naresh Kumar; George, Blassan P.; Chandran, Rahul; Im, Tynga; Houreld, Nicolette Nadene; Abrahamse, Heidi

doi:10.3390/antiox8120640

“…[ 34 ] High levels of ROS inhibit proliferation and reduce cell viability, while low levels of ROS stimulate signaling pathways involved in bone repair. [ 35–37 ] In this scenario, PBM therapy emerges as an alternative therapy to modulate the ROS expression, [ 38 ] and further investigations regarding the ROS modulation in this experimental model are necessary.…”

Section: Discussionmentioning

confidence: 99%

Recovering the osteoblastic differentiation potential of mesenchymal stem cells derived from diabetic rats by photobiomodulation therapy

Bueno

¹

,

Copete

²

,

Lopes

³

et al. 2020

Journal of Biophotonics

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Autologous cell‐based therapy for bone regeneration might be impaired by diabetes mellitus (DM) due to the negative effects on mesenchymal stem cells (MSCs) differentiation. Strategies to recover their osteogenic potential could optimize the results. We aimed to evaluate the effect of photobiomodulation (PBM) therapy on osteoblast differentiation of rats with induced DM. Bone marrow MSCs of healthy and diabetic rats were isolated and differentiated into osteoblasts (OB and dOB, respectively). dOB were treated with PBM therapy every 72 hour (660 nm; 0.14 J; 20 mW; 0.714 W/cm2, and 5 J/cm2). Cell morphology, viability, gene and protein expression of osteoblastic markers, alkaline phosphatase (ALP) activity, and the mineralized matrix production of dOB‐PBM were compared to dOB. PBM therapy improved viability of dOB, increased the gene and protein expression of bone markers, the ALP activity and the mineralized matrix production. PBM therapy represents an innovative therapeutic approach to optimize the treatment of bone defects in diabetic patients.

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“…Previous studies using PBM treatment for trauma and injury have shown that PBM decreases the activation of NF-kB (Rizzi et al 2006;Lee et al 2018). However, it is also postulated that ROS and NO generated by PBM treatment trigger the activation of NF-kB (Chen et al 2011;Kumar et al 2019). NO generation is hypothesized to occur when PBM activates CCO by displacement of NO, which generally inhibits CCO (Hamblin 2016).…”

Section: Pbm Treatment Activates a Multidimensional Stressmentioning

confidence: 99%

“…For instance, one of the proteins found to be activated by PBM in neurodegeneration models is the Rac1 GTPase (Song et al 2012;Meng et al 2013), a protein essential for axonal growth, stability, and phagocytosis. Rac1 inhibition causes actin dysfunction and motor neuron degeneration, but over-activation can cause the production of NOX-mediated ROS (D'Ambrosi et al 2014), triggering NF-kB (Chen et al 2011;Kumar et al 2019), causing the production and release of pro-inflammatory cytokines and oxidative stress (Liu et al 2017). Hence, the activation of Rac1 can either alleviate or exacerbate neurodegenerative disease conditions.…”

Section: Pbm Influences An Interconnected Network Of Cellular Signalimentioning

confidence: 99%

The Molecular Mechanisms of Action of Photobiomodulation Against Neurodegenerative Diseases: A Systematic Review

Bathini

¹

,

Raghushaker

²

,

Mahato

³

2020

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Neurodegenerative diseases might be slow but relentless, as we continue to fail in treating or delaying their progression. Given the complexity in the pathogenesis of these diseases, a broad-acting approach like photobiomodulation can prove promising. Photobiomodulation (PBM) uses red and infrared light for therapeutic benefits, working by stimulating growth and proliferation. The implications of photobiomodulation have been studied in several neurodegenerative disease models. It has been shown to improve cell survival, decrease apoptosis, alleviate oxidative stress, suppress inflammation, and rescue mitochondrial function. In in vivo models, it has reportedly preserved motor and cognitive skills. Beyond mitochondrial stimulation, the molecular mechanisms by which photobiomodulation protects against neurodegeneration have not been very well studied. This review has systematically been undertaken to study the effects of photobiomodulation at a molecular level and identify the different biochemical pathways and molecular changes in the process. The data showed the involvement of pathways like extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (MAPK), and protein kinase B (Akt). In addition, the expression of several genes and proteins playing different roles in the disease mechanisms was found to be influenced by PBM, such as neurotrophic factors and secretases. Studying the literature indicated that PBM can be translated to a potential therapeutic tool, acting through a spectrum of mechanisms that work together to decelerate disease progression in the organism, which is difficult to achieve through pharmacological interventions.

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“…PBM therapy and PBM has been shown to affect inflammation, inflammatory markers and cytokine production, and oxidative stress [ 24 – 27 ]. In the present study, we investigated the levels of cox-2, IL-6, and TNF- α postirradiation at 660 nm in diabetic wounded fibroblast cell culture models.…”

Section: Introductionmentioning

confidence: 99%

Levels of Cyclooxygenase 2, Interleukin‐6, and Tumour Necrosis Factor‐α in Fibroblast Cell Culture Models after Photobiomodulation at 660 nm

Shaikh-Kader

¹

,

Houreld

²

,

Rajendran

³

et al. 2021

Oxidative Medicine and Cellular Longevity

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Chemicals and signaling molecules released by injured cells at the beginning of wound healing prompt inflammation. In diabetes, prolonged inflammation is one of the probable causes for delayed wound healing. Increased levels of cyclooxygenase-2 (cox-2), interleukin–6 (IL-6), and tumour necrosis factor-alpha (TNF-α) are associated with the inflammatory response and in diabetes, and increased levels of these contribute to chronic wounds that do not heal. Rising levels of cox-2, IL-6, and TNF-α have also been associated with increased oxidative stress. Photobiomodulation (PBM) may impact wound healing processes by affecting the signaling pathways and molecules pertinent to tissue repair. In the present study, the effect of PBM (wavelength: 660 nm; energy density: 5 J/cm2) on levels of cox-2, IL-6, and TNF-α was determined in fibroblast cell culture models. Four WS1 models (normal, normal wounded, diabetic, and diabetic wounded) were irradiated at 660 nm, and the culture media was collected at 0, 24, and 48 h postirradiation. Cells that were not irradiated (0 J/cm2) served as the controls. The following parameters were determined postirradiation: cell morphology using light microscopy, cell viability using the Trypan Blue exclusion assay, and levels of the inflammatory markers cox-2, IL-6, and TNF-α were measured using ELISA. Cell migration increased in the wounded groups over the 48 h interval after PBM; viability improved postirradiation in the diabetic wounded groups at 0 and 24 h ( P ≤ 0.05 and P ≤ 0.01 , respectively); levels of cox-2 decreased in normal and diabetic wounded groups at 0 h ( P ≤ 0.001 ) and increased in the diabetic and diabetic wounded groups at 48 h postirradiation ( P ≤ 0.05 and P ≤ 0.01 , respectively), while levels of IL-6 decreased in the normal ( P ≤ 0.01 ), diabetic ( P ≤ 0.05 ), and diabetic wounded ( P ≤ 0.001 ) groups at 24 h and in the diabetic and diabetic wounded groups at 48 h ( P ≤ 0.05 ) postirradiation. TNF-α was decreased in the normal wounded groups ( P ≤ 0.05 ) at 48 h. Through its effect on decreased IL-6 levels in diabetic cell models, PBM at 660 nm may be successful at decreasing oxidative stress; however, the present study also found an increase in cox-2 levels at 48 h postirradiation.

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The Influence of Light on Reactive Oxygen Species and NF-кB in Disease Progression

Cited by 51 publications

References 106 publications

Recovering the osteoblastic differentiation potential of mesenchymal stem cells derived from diabetic rats by photobiomodulation therapy

Recovering the osteoblastic differentiation potential of mesenchymal stem cells derived from diabetic rats by photobiomodulation therapy

The Molecular Mechanisms of Action of Photobiomodulation Against Neurodegenerative Diseases: A Systematic Review

Levels of Cyclooxygenase 2, Interleukin‐6, and Tumour Necrosis Factor‐α in Fibroblast Cell Culture Models after Photobiomodulation at 660 nm

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