Photobiomodulation therapy on wound treatment subsequent to Q‐switched Nd: YAG laser tattoo removal in rat model

Imrigha, Nada Abusalah Almabrouk; Bidin, Noriah; Lau, Pik Suan; Musa, Nurfatin; Zakaria, Nurlaily; Krishnan, Ganesan

doi:10.1002/jbio.201600295

Cited by 14 publications

(8 citation statements)

References 15 publications

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“…Light power density was adjusted to be 0.1 W cm À2 and the light irradiation time was in 1 s -5 min interval (1 min of irradiation is equivalent to a dose of 6 J cm À2 , so the maximum irradiation dose was 30 J cm À2 ). These light power density and doses were chosen because red/NIR light with such parameters was shown to provide positive effects on cells and tissues, while not causing cell phototoxicity (1)(2)(3)(4)(5)(6)(7)(8)(31)(32)(33)(34)(35)(36).…”

Section: Methodsmentioning

confidence: 99%

“…Low-level light therapy (LLLT), or photobiomodulation (PBM), utilizes low-intensity red and near-infrared (NIR) light from specialized lasers or light-emitting diodes to treat a variety of human conditions (1). Multiple experimental and clinical studies on light treatment with red/NIR irradiation ranging from 600 to 1100 nm showed promising results for muscle recovery (2,3), wound healing (4,5), reduction of inflammation (1,6), pain (7), as well as neurotrauma and neurodegenerative diseases (8,9). In case of PBM, red/NIR light is absorbed by cytochrome c oxidase (CCO), resulting in the activation of mitochondria and the subsequent generation of reactive oxygen species (ROS) through a chain of reactions (10,11).…”

Section: Introductionmentioning

confidence: 99%

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Macrophages Modulated by Red/NIR Light: Phagocytosis, Cytokines, Mitochondrial Activity, Ca²⁺ Influx, Membrane Depolarization and Viability

Golovynska

Stepanov

Golovynskyi

et al. 2021

Photochem & Photobiology

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Low-level light therapy (LLLT) is emerging as a promising therapeutic approach to modulate the biochemical and molecular processes within living cells. LLLT is known to produce local and systemic effects; therefore, immune cells in local tissues or in the circulation are affected by light. However, this specific effect remains weakly explored. In this study, the effect of red (650 nm) and NIR (808 nm) light on phagocytosis (respiratory burst), cytokine expression, mitochondrial activity, ROS generation, Ca 2+ influx and membrane depolarization in macrophages in vitro is investigated. Both the phagocytic capacity and adhesion of macrophages strongly (~2.5 times) increased in the first hours after exposure to light in a dose-dependent manner. The light-evoked upregulation of phagocytosis is found to be less efficient than the maximal pharmacologically induced enhancement of ~3.2 times. Also, red/NIR light reduces the production of pro-inflammatory cytokines and activates the secretion of anti-inflammatory cytokines by several times in activated macrophages. At the same time, the viability shows a biphasic dose response: it increases after irradiation with lower doses (0.3-1 J cm À2 ) and decreases after treatment with higher doses (18-30 J cm À2 ), which is apparently associated with the upregulation of ROS generation, followed by an increase in the mitochondrial activity.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Macrophages Modulated by Red/NIR Light: Phagocytosis, Cytokines, Mitochondrial Activity, Ca²⁺ Influx, Membrane Depolarization and Viability

Golovynska

Stepanov

Golovynskyi

et al. 2021

Photochem & Photobiology

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“…Light power density was adjusted to be 30 mW/cm 2 and the light irradiation time was for 5 min, resulting in the irradiation dose of nearly 10 J/cm 2 . These light power density and doses were chosen because NIR light with such parameters was shown to provide positive effects on cells and tissues, while not causing cell phototoxicity [44][45][46][47][48][49][50][51][52].…”

Section: Light Treatmentmentioning

confidence: 99%

Near-infrared light reduces β-amyloid-stimulated microglial toxicity and enhances survival of neurons: Mechanisms of light therapy for Alzheimer's disease

Stepanov

Golovynska

Zhang

et al. 2022

Preprint

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Background. Low-intensity light can decelerate neurodegenerative disease progression and reduce amyloid β (Aβ) levels in the cortex, though, the cellular and molecular mechanisms by which photobiomodulation protects against neurodegeneration are still in the early stages. Microglia cells play a key role in the pathology of Alzheimer's disease by causing chronic inflammation. We present new results concerning the photobiomodulation of both oxidative stress and microglia metabolism associated with the activation of metabolic processes by 808 nm near-infrared light. Methods. The studies were carried out using healthy male mice to obtain the microglial cell suspension from the hippocampus. Oligomeric β-amyloid (1–42) was prepared and used to treat microglia cells. Light irradiation of cells was performed using diode lasers emitting at 808 nm (30 mW/cm2 for 5 min, resulting in the dose of 10 J/cm2). Mitochondrial membrane potential, ROS level studies, cell viability, apoptosis and necrosis assays were performed using epifluorescence microscopy. Phagocytosis, nitric oxide and H2O2 production, arginase and glucose 6-phosphate dehydrogenase activities were measured using standard assays. Cytokines, glucose, lactate, and ATP were measurements with ELISA. As our data were normally distributed, Student’s t-test was used. Results. The light induces a metabolic shift from glycolysis to mitochondrial activity in pro-inflammatory microglia affected by oligomeric Aβ. Thereby, the level of anti-inflammatory microglia increases. This process is accompanied by a decrease in pro-inflammatory cytokines and an activation of phagocytosis. Light exposure decreases the Aβ-induced activity of glucose-6-phosphate dehydrogenase, an enzyme that regulates the rate of the pentose phosphate pathway, which activates nicotinamide adenine dinucleotide phosphate oxidases to further produce ROS. During co-cultivation of neurons with microglia, light prevents the death of neurons, which is caused by ROS produced by Aβ-altered microglia. Conclusions. These original data clarify reasons for how photobiomodulation protects against neurodegeneration and support the use of light for therapeutic research in the treatment of Alzheimer's disease.

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“…Selective absorption of the laser light by the pigments results in fragmented tattoo particles which allows transportation of the tinier fragments away from the skin via phagocytosis [ 36 , 38 ]. Tattoo removal by lasers typically causes postprocedure open wounds on the treated skin due to the high energy of the intense light pulses [ 38 ].…”

Section: Types Of Wounds and Process Of Repairmentioning

confidence: 99%

Dexpanthenol in Wound Healing after Medical and Cosmetic Interventions (Postprocedure Wound Healing)

et al. 2020

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With the availability of new technologies, the number of subjects undergoing medical and cosmetic interventions is increasing. Many procedures (e.g., ablative fractional laser treatment) resulting in superficial/minor wounds require appropriate aftercare to prevent complications in wound healing and poor cosmetic outcome. We review the published evidence of the usefulness of topical dexpanthenol in postprocedure wound healing and the associated mechanisms of action at the molecular level. A search in the PubMed and Embase databases was performed to query the terms dexpanthenol, panthenol, superficial wound, minor wound, wound healing, skin repair, and postprocedure. Search results were categorized as clinical trials and in vitro studies. In vitro and clinical studies provided evidence that topically applied dexpanthenol promotes superficial and postprocedure wound healing. Latest findings confirmed that dexpanthenol upregulates genes that are critical for the healing process. The gene expression data are of clinical relevance as evidenced by prospective clinical studies indicating that topical dexpanthenol accelerates wound healing with rapid re-epithelialization and restoration of skin barrier function following skin injury. It can therefore be inferred that topical dexpanthenol represents an appropriate and state-of-the-art treatment option for superficial postprocedure wounds, especially when applied early after the superficial skin damage.

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Photobiomodulation therapy on wound treatment subsequent to Q‐switched Nd: YAG laser tattoo removal in rat model

Cited by 14 publications

References 15 publications

Macrophages Modulated by Red/NIR Light: Phagocytosis, Cytokines, Mitochondrial Activity, Ca²⁺ Influx, Membrane Depolarization and Viability

Macrophages Modulated by Red/NIR Light: Phagocytosis, Cytokines, Mitochondrial Activity, Ca²⁺ Influx, Membrane Depolarization and Viability

Near-infrared light reduces β-amyloid-stimulated microglial toxicity and enhances survival of neurons: Mechanisms of light therapy for Alzheimer's disease

Dexpanthenol in Wound Healing after Medical and Cosmetic Interventions (Postprocedure Wound Healing)

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Photobiomodulation therapy on wound treatment subsequent to Q‐switched Nd: YAG laser tattoo removal in rat model

Cited by 14 publications

References 15 publications

Macrophages Modulated by Red/NIR Light: Phagocytosis, Cytokines, Mitochondrial Activity, Ca2+ Influx, Membrane Depolarization and Viability

Macrophages Modulated by Red/NIR Light: Phagocytosis, Cytokines, Mitochondrial Activity, Ca2+ Influx, Membrane Depolarization and Viability

Near-infrared light reduces β-amyloid-stimulated microglial toxicity and enhances survival of neurons: Mechanisms of light therapy for Alzheimer's disease

Dexpanthenol in Wound Healing after Medical and Cosmetic Interventions (Postprocedure Wound Healing)

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Product

Resources

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Macrophages Modulated by Red/NIR Light: Phagocytosis, Cytokines, Mitochondrial Activity, Ca²⁺ Influx, Membrane Depolarization and Viability

Macrophages Modulated by Red/NIR Light: Phagocytosis, Cytokines, Mitochondrial Activity, Ca²⁺ Influx, Membrane Depolarization and Viability